











Class T?C, (n 9. 1 
Book H 5 
Copyright N?__ 

COPYRIGHT DEPOSrr. 


















Pulmonary artery 


Left auricle 


Right auricle 


Superior vena cava 


Ascending aorta 


Vena cordis 
magna 

Anterior de¬ 
scending 
branch of left 
coronary 
artery 


Anterior 

longitudinal 

sulcus 




Left branch of 
pulmonary artery 


Vena cordis 1 
anterior g 

Right 

coronary 
artery 


Vena cordis 
anterior 


Innominate artery 


Left subclavian artery 
Left common carotid artery 


Left ventricle 


Right ventricle 


Fig. L The heart viewed from above and in front. The surface vessels have been injected. 
(Spalteholz : Handatlas der Anatomie.) 





THE HEART 

IN 

MODERN PRACTICE 

DIAGNOSIS AND TREATMENT 


BY 

WILLIAM DUNCAN REID, A.B., M.D. 

CHIEF OF HEART CLINIC AT THE BOSTON DISPENSARY, JUNIOR ASSISTANT VISITING PHYSICIAN AND MEMBER 
OF THE HEART SERVICE AT THE BOSTON CITY HOSPITAL, FORMERLY ASSISTANT VISITING 
PHYSICIAN TO OUT-PATIENTS AT THE MASSACHUSETTS GENERAL HOSPITAL. 


32 ILLUSTRATIONS 




PHILADELPHIA AND LONDON 
J. B. LIPPINCOTT COMPANY 


““RCtsi 

TR5- 


COPYRIGHT, 1923, BY J. B. LIPPINCOTT COMPANY 



PRINTED BY J. B. LIPPINCOTT COMPANY 
AT THE WASHINGTON SQUARE PRESS 
PHILADELPHIA, U. 8 . A. 

©Cl A7 05133 


APR 27 ^3 


w* 


TO MY FATHER 


ROBERT ALEXANDER REID, M.D. 




PREFACE 

It is well known that since the introduction of graphic 
methods of examination, extensive advances have been 
made in the knowledge of the heart in health and disease. 
Unfortunately, an acquaintance with this progress in cardi¬ 
ology can be gained only by a rather wide reading of the 
literature, as, at present, I am aware of no single book in 
English which is suitable to recommend to the student or 
physician who asks for the name of a single volume in 
w r hich he may read up on the subject. The interest in the 
study of the abnormal rhythms of the heart has been so 
great that many of the recent authors have limited them¬ 
selves to a presentation, often admirable it is true, of this 
aspect alone. There seems, then, in my opinion, to be a 
real need for a book which will incorporate the best of the 
new knowledge with that less recently acquired but which 
may be said to have stood the test of time. Such a book 
should preferably be brief enough as to be attractive to 
the bulk of the profession, whose opportunity to read upon 
a single aspect of medicine is limited. This little book is 
offered as an attempt, perhaps with indifferent success, to 
fill the above-mentioned need. 

The attention of the reader is invited to the method in 
which the subject is presented. I refer to the division 
of the main part of the book into three sections, in which 
heart disease is described from an etiological, a functional, 
and a structural viewpoint, respectively. The importance 
of etiology does not receive sufficient emphasis when it is 
mentioned only in teaching or in an article contributed to 

5 


6 


PREFACE 


a medical journal, but if we believe in it, and we do, the 
text-book should be written in a method that will stamp 
this on the reader’s mind. For instance, is it surprising 
that the average physician is hazy as to the effects of 
syphilis on the circulatory organs when it is realized that 
to find out what is known he must turn to the chapter on 
valvular affections for an account of aortic regurgitation, 
to another for syphilitic myocarditis, to another for heart- 
block and other arrhythmias occurring in syphilis, and to 
still others for aneurism and angina pectoris? Logically, 
this material should be brought together in some such man¬ 
ner as I have attempted in the chapter on “Cardiovascular 
Syphilis ” The day of the consideration of heart affections 
from the viewpoint of the structural change or anatomical 
lesion has passed; of greater importance is that of the 
functional condition and perhaps even more essential, to 
an intelligent conception, is the recognition of the etiolog¬ 
ical type. I have endeavored to present the subject as 
nearly in conformance with the above belief as is practi¬ 
cable. My excuse for insisting on this point is that it has 
been made a major feature of this book, which differs 
thereby from any other book with which I am acquainted. 

It may appear that a proper balance has not been main¬ 
tained between the different subjects. Thus, the chapter 
on “ Artenosclerotic Heart Disease” is of equal length 
with that on “Septic Heart Disease ” though the former is 
of infinitely greater frequency and importance. However, 
certain subjects lend themselves to a brief presentation, 
while with others clearness demands greater space. I 
have sought for brevity with clearness. 

Much as it is desirable, it was not found possible to 
avoid controversial subjects; cardiology is in process of 


PREFACE 


7 


change and physicians are not in agreement on all points. 
Whenever a point might be new to some readers, authority 
has been quoted. It is hoped that the references might 
stimulate collateral reading. 

The electrocardiograms were made by the author in the 
laboratory of the Boston City Hospital. 

It is a pleasure to acknowledge thanks to Austin W. 
Cheever, who kindly suggested most of the details of the 
antisyphilitic treatment recommended for cardiovascular 
syphilis. 


W. D. R. 




CONTENTS 

SECTION I 

PRELIMINARY CONSIDERATIONS 

CHAPTER PAGE 

I. Anatomical, Physiological, and Embryological Considerations.. 15 

II. Methods of Examination. 31 

III. Methods of Examination (cont.)—Polygraphic Examination_ 49 

IV. Methods of Examination (concl.)—Electrocardiographic Ex¬ 

amination . 64 

V. The Normal Heart. 84 

VI. The Classification of Heart Disease. 91 

SECTION II 

TYPES OF HEART DISEASE (ETIOLOGIC) 

VII. Rheumatic Heart Disease. 97 

VIII. Septic Heart Disease. 119 

IX. Cardiovascular Syphilis. 126 

X. Arteriosclerotic Heart Disease. 142 

XI. Hypertensive Heart Disease. 149 

XII. The Heart in Hyperthyroidism. 160 

XIII. The Heart in Diphtheria. 165 

XIV. Congenital Heart Disease. 170 

XV. Effort Syndrome : Irritable Heart. 175 

SECTION III 

FUNCTIONAL CONDITIONS 

XVI. Heart Failure—Angina Pectoris. 183 

XVII. The Arrhythmias. 195 

SECTION IV 

STRUCTURAL LESIONS 

XVIII. Structural Lesions. 225 

SECTION V 

XIX. Treatment . 247 

APPENDIX 

Illustrative Case Reports.273 


9 






















LIST OF ILLUSTRATIONS 

no. PAGE 

1. Anterior view of heart. frontispiece 

2. Heart with part of interior exposed by the removal of a slice from the 

anterior surface. 18 

3. Curves of pressure in the left ventricle and right auricle. 24 

4. Comparison between percussion and teleradiography in the determination of 

the left cardiac border. 37 

5. Arteriograms of pulsus altemans, and of pseudo-alternation. 52 

6. Normal polygram. 52 

7. Sinus arrhythmia. 52 

8. 9. Auricular premature beats. Ventricular premature beat. 58 

10. Paroxysmal tachycardia of auricular origin. 58 

11. Auricular fibrillation. 59 

12. Partial heart-block. 62 

13. Complete heart-block. 62 

14. The Einthoven triangle. 69 

15. Normal electrocardiogram. 70 

16. Ventricular preponderance. 71 

17. Sinus arrhythmia. 74 

18. Auricular premature beats. 75 

19. Ventricular premature beats. 76 

20. Paroxysmal tachycardia. 77 

21. Auricular flutter. 78 

22. Auricular fibrillation. 79 

23. Partial heart-block. 80 

24. Complete auriculo-ventricular heart-block, and intraventricular block.... 81 

25. Combined arrhythmias. 83 

26. Spirochetes in the myocardium. 126 

27. Syphilitic myocarditis. 127 


11 



























PLATES 


PLATE PAGE 

1. Rheumatic heart disease; healed mitral endocarditis with calcification 

and rupture. Note the thickening and shortening of the chordae 
tendineae. 98-99 

(Courtesy of Timothy Leary) 

2. Rheumatic heart disease; acute infectious lesion of branch of the coronary 

artery with surrounding myocarditis. 98-99 

(Courtesy of Frank B. Mallory) 

3. Large vegetations on the mitral valve, in septic heart disease due to the 

pneumococcus. 120-121 

(Courtesy of Frank B. Mallory) 

4. Aneurism of the wall of the left ventricle with thrombus inside, associated 

with coronary sclerosis and hypertensive heart disease. 244-245 

(Courtesy of Frank B. Mallory) 

5. Thrombi in the auricle. Note the corrugated surface of the large 

thrombus. 270-271 

(Courtesy of Frank B. Mallory) 


12 







SECTION I 

PRELIMINARY CONSIDERATIONS 



THE HEART IN 
MODERN PRACTICE 

CHAPTER I 

ANATOMICAL, PHYSIOLOGICAL, AND EMBRYO- 
LOGICAL CONSIDERATIONS 

The following salient points of cardiac anatomy, phys¬ 
iology, and embryology have been selected as of most value 
in the clinical understanding of the heart. 

ANATOMY 

The heart is a somewnat conical-shaped mass of muscle, 
occupying the pericardial cavity in the middle mediasti¬ 
num. It is placed obliquely in the thorax; the base is 
directed backwards and corresponds to the fifth to eighth 
thoracic vertebras inclusive, while the apex points down¬ 
ward, forward, and to the left, at a level between the fifth 
and sixth costal cartilages and a little inside the left mid- 
clavicular line. 

The heart cavity is divided into two lateral halves, and 
a transverse constriction further divides these latter into 
two cavities, the posterior on the two sides being called the 
auricles and the anterior the ventricles. The division of 
the heart into the four cavities is indicated by grooves upon 
its surface. In the groove indicating the auriculo-ventric- 
ular septum lie the main trunks of the nutrient vessels of 
the heart. 

The right auricle is composed of a posterior and 
larger portion, the sinus venosus., and a smaller cavity 

15 


16 


MODERN CONCEPTION OF HEART DISEASE 


placed in front and above, the right auricular appendix. 
Into the sinus venosus empty the superior and inferior 
vena? cava?, and its mesial wall is formed by the inter- 
auricular septum. 

The Left Auricle is smaller than the right. It, too, 
consists of a principal cavity and an auricular appendix. 
The left auricular appendix is directed forward and to the 
right so that it overlaps the root of the pulmonary artery. 
The pulmonary veins, usually four but sometimes three in 
number, open into the upper part of the posterior wall 
of the left auricle. 

The Ventricles are larger and the muscular layer 
forming their walls is much thicker than is that of the auri¬ 
cles. The right ventricle extends from the right auricle 
to near the apex and forms the larger part of the anterior 
surface of the heart. At its base, the right ventricle is 
prolonged into a conical pouch, the conus arteriosus or 
infundibulum, from which the pulmonary artery has 
its origin. 

The left ventricle is longer than the right, beyond which 
it projects to form the apex of the heart. It appears on 
the anterior cardiac surface as a narrow strip along the 
left border, but forms a considerable portion of the postero- 
inferior surface. The thickness of the muscular wall of 
the left ventricle averages about three times that of the 
right ventricle. 

Valves. —There are four valves in the heart, two be¬ 
tween the auricles and ventricles and two between the ven¬ 
tricles and the aortic and pulmonary arteries. These valves 
are formed by a reduplication of the endocardium and 
strengthened inside by a fibrous layer. At the attachment of 
each valve is an annular ring of dense fibrous tissue. The 


ANATOMICAL CONSIDERATIONS 


17 


cusps of the auriculo-ventricular valves are connected at 
their free margin by the chordae tendineae to the papillary 
muscles. These fibrous bands, or chordae tendineae, by 
limiting the play of the cusps, serve to prevent invagination 
of the latter into the auricles at the time of ventricular 
contraction. In the right heart, the valve has three sec¬ 
tions or cusps and hence its name, tricuspid. That of the 
left side has but two cusps and it is termed the bicuspid 
or mitral valve. 

The Aortic and Pulmonary Valves each consist of 
three semilunar segments or cusps, the inner margins of 
which are free. Near the centre of the free margins of 
each cusp is a small nodule of fibrous tissue, termed the 
corpus Aurantii. These latter are to be distinguished 
from the thickenings produced by endocarditis. At the 
base of the aorta and of the pulmonary artery are small 
dilatations opposite each of the semilunar valve segments. 
These are known as the sinuses of Valsalva. 

The Myocardium consists of bands and layers of 
muscle tissue intricately interlaced. The fibres of the 
bundle of His are the only fibres that are common to both 
auricle and ventricle. MacCallum’s studies of the myo¬ 
cardium have disclosed that by dissection the heart may be 
unrolled so that the four chambers can be separated and 
weighed separately, a matter of importance in careful 
studies of ventricular hypertrophy. 

The Sino-auricular Node is a small mass of special¬ 
ized tissue located at the junction of the superior vena cava 
with the right auricle and immediately below the endo¬ 
cardium. This node is the seat of origin of the normal 
heart beat. 


18 MODERN CONCEPTION OF HEART DISEASE 

The Auriculo-ventricular Bundle of His (Fig. 
2) is the only direct muscle connection between the auricles 
and ventricles. It arises from near the opening of the 



Fig. 2.—Heart with part of interior exposed by the removal of a slice from the anterior surface. 
The auriculo-ventricular conduction bundle is represented schematically. 


S. C.—Superior Cava. 

P. A.—Pulmonary Artery. 

R. A.—Right Auricle. 

I. C.—Inferior Cava. 

1. Auriculo-ventricular Node. 

2. Bundle of His. 


3. Right Branch. 9. Pulmonic Valve. 

4. Left Branch. 10. Mitral Valve. 

5. Right Auricular Appendage. 11. Papillary Muscle. 

6. Tricuspid Valve. 12. Right Ventricle. 

7. Interventricular Septum. 13. Left Ventricle. 

8. Aortic Valve. 14. Cut Surface of Ventricular Vail. 

( Gray'a: Anatomy, somewhat modified.) 


coronary sinus, where it is connected with the annular and 
septal fibres of the right auricle. These fibres converge, 
form anode (node of Tawara), and continue as a compact 






ANATOMICAL CONSIDERATIONS 


19 


bundle which passes forward to the upper limit of the 
muscle portion of the ventricular septum, where it divides 
into right and left branches. These latter course down 
on either side of the ventricular septum to the right and 
left ventricles, respectively. Each limb is enclosed in a 
layer of connective tissue which isolates it from the mus¬ 
culature of the interventricular septum, but in the lower 
part of the ventricles each branch separates into numerous 
strands which enter the papillary muscles and spread over 
the entire inner surface of the ventricular muscle and form 
histological connections with the true cardiac muscle fibres. 
The right limb is the smaller of the two and usually enters 
the anterior papillary muscle by passing along the modera¬ 
tor band when that is present. The bundle of His consists 
of narrow, somewhat fusiform fibres, but the two branches 
and their terminal strands are composed of Purkinje fibres. 

A bursa or lubricating mechanism is in relation with 
the main bundle, according to Curran , 1 and a special artery 
arising from the right coronaiy enters and follows the 
bundle. These facts suggest the possibility of the occur¬ 
rence of a bursitis from acute articular rheumatism or 
other infections, as causing certain cardiac symptoms. 

The Purkinje Fibres are very much larger than the 
cardiac cells, and differ from them in several ways. In 
longitudinal section they are quadrilateral in shape. The 
central portion of each fibre contains one or more nuclei 
and is made up of granular protoplasm, with no indication 
of striations, while the peripheral portion is clear and has 
distinct cross striations. The fibres are intimately con¬ 
nected with each other, possess no definite sarcolemma, 
and do not branch. 


1 The Anatomical Record, 1909, vol. iii, No. 12: 618. 



20 


MODERN CONCEPTION OF HEART DISEASE 


The Arteries supplying the heart are the right and 
left coronaries. The right coronary artery rises from the 
anterior aortic sinus of Valsalva, passes forward to the 
auriculo-ventricular groove and after coursing to the right, 
divides into a transverse branch, which continues in the 
auriculo-ventricular groove to anastomose with the trans¬ 
verse branch of the left coronary artery, and a descending 
portion which supplies the right and posterior surface of 
the heart and finally anastomoses with the descending 
branches of the left coronary at the apex. 

The left coronary has its origin in the left posterior 
sinus of Valsalva of the aorta. It, too, divides into a trans¬ 
verse and a descending branch. The former passes to the 
left in the auriculo-ventricular groove to anastomose with 
its fellow from the right coronary, and the descending 
branch, after supplying the left and part of the anterior 
cardiac surface, descends to the anastomosis at the apex. 

These vessels occasionally arise by a common trunk 
or their number may be increased to three or more. 

Veins. —The coronary sinus receives the majority of 
the veins draining the blood from the substance of the 
heart. It terminates in the right auricle between the 
opening for the inferior vena cava and the tricuspid 
valve. Its orifice is guarded by a semilunar valve (the 
coronary valve). 

The anterior cardiac veins, comprising three or four 
small vessels, empty direct into the right auricle. The 
veins of Thebesius, consisting of a number of minute ves¬ 
sels arising in the substance of the heart, empty mostly into 
the auricles, but a few empty into the ventricles. 

The Nerves of the heart are derived from the super¬ 
ficial and the deep cardiac plexuses, and from these plex- 


ANATOMICAL CONSIDERATIONS 


21 


uses obtain fibres from the vagus and sympathetic nerves. 
The superficial cardiac plexus lies under the arch of the 
aorta, while the deep cardiac plexus is under the tracheal 
bifurcation. The nerves from the plexus are freely dis¬ 
tributed on the surface and in the substance of the heart, 
many of the separate filaments being furnished with 
small ganglia. 

The Pericardium is a serofibrous sac in which the 
heart and the commencement of the great vessels are con¬ 
tained. It consists of an outer fibrous layer and an inner 
layer of serous type. The fibrous layer blends with the 
central portion of the diaphragm and with the external 
coat of the great vessels. There are several prolongations 
of this outer layer (called ligaments of the pericardium) 
which attach it to the sternum, diaphragm, and vertebral 
column (by way of the cervical fascia). On the lateral 
surface of the pericardium is found the phrenic nerve as 
it passes downward to the diaphragm. The serous layer 
lines the fibrous pericardium and is invaginated by the 
heart so that it is described as consisting of a parietal and 
of a visceral layer. 

The Internal Mammary Arteries, to be avoided in 
paracentesis of the pericardium, descend on the inner tho¬ 
racic wall about one half an inch from the sternal margins. 

The Pulmonary Artery rises from the conus arteri¬ 
osus slightly anterior and to the left of the aorta. It 
passes obliquely to the left and under the arch of the 
aorta, where it divides into right and left branches. The 
artery averages but two inches in length. It is connected 
to the aortic arch by a short fibrous cord, the ligamentum 
arteriosum. This latter is the remnant of the fetal 
ductus arteriosus. 


22 


MODERN CONCEPTION OF HEART DISEASE 


The Aorta rises from the base of the left ventricle, 
ascends a short distance, then arches backward and to the 
left to descend on the left side of the vertebral column. 
The ascending portion starts behind the left half of the 
sternum at the level of the lower border of the third costal 
cartilage and passes upward and forward to the right 
to the level of the upper border of the second right costal 
cartilage. The ascending portion is contained within the 
pericardium. When the aorta is distended it is about one 
quarter of an inch from the posterior surface of the 
sternum. This space is occupied by loose areolar tissue 
and the remains of the thymus gland. 

The transverse arch of the aorta lies upon the trachea, 
esophagus, and thoracic duct, and the left recurrent laryn¬ 
geal nerve winds around it. 

PHYSIOLOGY 

The Events That Occur During a Single Car¬ 
diac Cycle.— A complete cardiac cycle is the time from 
any given feature of the heart beat until that feature is 
again produced. For example, if we begin with the clos¬ 
ure of the semilunar valves, the sequence of events is as 
follows:—At that moment the second heart sound is heard 
and the ventricle is quickly relaxing from its previous 
contraction. For a brief interval the auriculo-ventricular 
valves remain closed and for the moment the ventricles are 
shut off on both sides. The blood is flowing steadily into 
the auricles and dilating them. As soon as the ventricles 
relax completely the pressure of the blood in the auricles 
presses open the auriculo-ventricular valves, and from that 
moment until the beginning of auricular systole the blood 
from the large veins is filling both auricles and ventricles. 


PHYSIOLOGICAL CONSIDERATIONS 


23 


The ventricular walls become more tense and the auriculo- 
ventricular valves are floated into position ready for 
closure. The auricular systole sends a sudden wave of 
blood into the ventricles, which closes the auriculo-ventric- 
ular valves . 2 The contraction of the auricles also momen¬ 
tarily blocks or retards the flow from the large veins, 
whence the auricular wave in the jugular veins. Ventric¬ 
ular systole follows immediately upon auricular systole. 
As the ventricles enter into contraction, the first sound 
is audible, and for a brief moment the ventricular cavities 
are again shut off on both sides. Soon the rising intra¬ 
ventricular pressure opens the semilunar valves and a 
stream of blood is forced into the aorta and pulmonary 
artery. During ventricular systole, the auricles continue 
to receive blood from the large veins; the venous flow is 
never completely blocked, but at most experiences a slight 
retardation during the very brief auricular systole. At 
the end of ventricular systole the intraventricular pressure 
falls below that in the aorta and pulmonary artery and the 
excess of arterial pressure closes the semilunar valves, thus 
completing the cardiac cycle. 

Study of the diagram, Fig. 3, showing the relation of 
the pressure in the auricle, ventricle, and aorta, should aid 
one to visualize the events in a cardiac cycle. The latter 
is commonly divided into two periods: that of contraction 
or systole, and that of relaxation or diastole. At an aver¬ 
age heart rate of 72 per minute, the cardiac cycle occupies 
about 0.8 of a second, and this may be divided approxi¬ 
mately as follows: auricular systole 0.1, ventricular systole 
0.3, and the common pause of the heart as 0.4 of a second, 
respectively. Diastole, as commonly determined, is the 


2 Henderson, Y., and Johnson, F. E.: Heart, 4:69, 1912-1913. 



24 


MODERN CONCEPTION OF HEART DISEASE 


period of ventricular diastole, and auricle systole is de¬ 
scribed as late diastolic or presystolic. In hearts beating 
at a slow rhythm, the greater part of ventricular filling may 
be completed in early diastole, which is then followed by 



Fig. S.—Curves of pressure in the left ventricle and right auricle; the radial and jugular pulse 
tracings are placed above and below to show their time-relations. 

A. V. C. and A. V. O., closure and opening of the auriculo-ventricular valves, respectively; S. O. 
and S. C., opening and closure of semilunar valves, respectively; pr., presphygmic period; po., post- 
sphygmic period. The time intervals of some of the periods are marked above and below in seconds. 

(This diagram is from one published by Thomas Lewis, with slight modification.) 

a period of comparative rest. This resting phase is 
termed diastasis. 

Contrary to the general impression, the apex of the 
heart, from which the pericardium has not been removed, 
does not twist forward and to the right with contraction, 
but, according to Starling , 3 there is then a definite descent 


Starlixg, E. H.: Human Physiology, third edition, 1920, p. 947. 














PHYSIOLOGICAL CONSIDERATIONS 


25 


of the base downward toward the apex. The heart tends 
to be fixed by its attachment to the vena? cava?. This fact 
is a factor in an enlargement of the right ventricle being 
manifest to the left rather than to the right. 

The Heart Sounds. —The first heart sound is largely 
muscular in origin. It begins with the “setting” of the 
ventricles, and continues until the highest intraventricular 
pressure has been produced. The systole of the ventricles 
then continues in silence the discharge of blood into the 
aorta until its sudden termination, which is marked by the 
second sound. The second sound is associated with the 
closure of the aortic and pulmonary valves. The actual 
sound is due to the relaxed semilunar cusps suddenly being 
put into a state of tension; a comparable somid may be pro¬ 
duced by suddenly drawing taut a fold of a handkerchief 
held between one’s hands. A second sound is possible with¬ 
out a perfect closure of the valve. The closure of the 
mitral and tricuspid valves is relatively quiet and probably 
contributes but little to the volume of the first heart sound . 4 
The loudness and intensity of the first sound has been 
found 5 to be directly proportional to the intracardiac ten¬ 
sion, and especially to the tension developed during the 
isometric period i.e ., before the opening of the semilunar 
valves. 

Mechanism of the Heart Beat. —On inspection the 
exposed heart is seen to contract and relax in rhythmic 
succession. The contraction wave starts at rhythmic 
intervals at the sino-auricular node, then spreads centrifu- 
gally over the auricles, like the rings from a stone thrown 
into a millpond, meets a slight delay at the auriculo-ven- 

* Reid, W. D.: Jour. Amer. Med. Assn., 76: 432 (Feb. 12, 1921). 

1 Wiggees, C. J.: Arch. Jnt. Med., 24:471 (Nov., 1919). 





26 


MODERN CONCEPTION OF HEART DISEASE 


tricular bundle, and thence proceeds through the right and 
left branches to the Purkinje fibres, where it is distributed 
to the muscular fibres of the ventricular walls. Other 
parts of the specialized tissue, namely, the auriculo- 
ventricular (Tawara) node and the conduction bundle 
on the ventricular side of the node, have the power of 
stimulus production, but the rate of this is slower than that 
of the sino-auricular node, and therefore, save in abnormal 
conditions, the heart contracts in response to stimuli 
received from the higher centre, the sino-auricular node. 

It now seems established that the myogenic theory of 
the production and transmission of the heart beat is correct. 
The nerves have been shown to control the heart beat but 
do not initiate it or conduct the contraction wave. The 
vagus inhibits and the sympathetic accelerates the beat, 
each counteracting the other. The heart with its nerve 
connections severed may continue to beat. 

Immediately after the muscle fibres of the heart have 
contracted they exhibit a refractory stage in that they fail 
to respond to stimulation. Restoration of excitability at 
once commences and increases progressively during dias¬ 
tole. When the cardiac muscle is stimulated it either does 
not contract at all, or does so to the fullest possible extent 
at the time. The amount of contraction does not depend 
on the strength of the stimulus employed, but varies 
according to the time at which the stimulus is received. 
When a stimulus is received early in diastole the resulting 
contraction is weaker than that of the previous cardiac 
cycle. Within limits, the amount of contraction varies 
directly in proportion to the length of the previous diastole. 
This principle serves to explain the fact that the more 


PHYSIOLOGICAL CONSIDERATIONS 


27 


rapid the heart rate the greater is the possibility of 
cardiac failure. 

Gaskell has described five fundamental functions of 
cardiac muscle, namely: stimulus production, excitability, 
conductivity, contractility, and tonicity. The terms are 
somewhat theoretical, to be sure, but very useful in the dis¬ 
cussion of the various features of the heart’s activity. In 
abnormal conditions of the heart it is rare that the disturb¬ 
ance is limited to but one of the five fundamental functions 
mentioned above. 

The Physiology of Muscular Exercise. —The out¬ 
put of the heart varies from 3 to 5 litres per minute in 
individuals at rest, it is raised by moderate exercise to 8 
or 9 litres, and during heavy muscular exercise it may reach 
20 litres or even more. It is of importance to consider 
briefly the conditions associated with this increase in the 
cardiac output. 

At the onset of exercise, a constriction of the splanchnic 
vessels takes place and this diverts much of the blood into 
the muscles, and increases the pressure in their vessels. 
The increase in the blood supplied to the active muscles 
enables the latter, by their contractions, to expel a greater 
volume of blood into the veins and thence back to the 
heart. The heart then drives the blood out again into the 
muscles. Thus, in a certain sense, it can be seen that the 
mechanism, by which during exercise a greater volume of 
blood circulates through the active muscles, is largely de¬ 
pendent upon the activity of the latter. If the exercise 
is continued, some dilatation of the vessels in the working 
muscles usually occurs, and this results in a further in¬ 
crease in the blood supplied to these same muscles and 
enables them to return more blood to the heart. 


28 


MODERN CONCEPTION OF HEART DISEASE 


It has been said above that during exercise there is a 
greater volume of blood returned to the heart, which is 
then called upon to propel it forward if the increased cir¬ 
culation is to be maintained. In other words, the output 
of blood from the heart must be augmented. The physi¬ 
ologists state that this may be accomplished by an increase 
in the number of contractions per minute and by a greater 
output per beat. The former certainly occurs, but as 
regards the latter there is some disagreement. 

During diastole the heart is filled passively by the blood 
flowing in from the veins, and if the pressure of the latter 
is increased (in exercise) the heart undergoes a greater 
distention or dilatation. Dilatation is, therefore, a per¬ 
fectly normal process, and the extent to which it can take 
place, under physiological conditions, is ultimately limited 
by the pericardium. * 6 

It has been shown 7 that the ventricles never pass in a 
single systole from utmost fulness to extreme contraction. 
The same observers hold that under normal conditions [i.e., 
when the pressure of the venous return is not decreased) 
the amplitude of the beat is determined by the duration of 
diastole; in other words, the systolic discharge is less when 
the heart rate is accelerated. The output per beat may be 
increased, however, during exercise when the heart rate is 
not quickened, as apparently occurs in individuals habitu¬ 
ated to exercise. 

An understanding of the physiology of exercise makes 
more intelligible many of the phenomena observed in the 
study of the heart both in health and in disease. The 

0 Bainbridge, F. A.: The Physiology of Muscular Exercise, Longmans, 

Green and Co., 1919, p. 54. 

7 Henderson, Y., and Barringer, T. B., Jr.: Amer. Jour. Physiol., xxx:366 
(March, 1913). 



EMBRYOLOGICAL CONSIDERATIONS 


29 


subject is, unfortunately, complex and further presenta¬ 
tion will not be attempted here. 

EMBRYOLOGY 

The Circulatory System in the early embryo is that 
of a single tube or artery whose wall at a certain point 
possesses the power of rhythmic contractions. The spe¬ 
cialized part of this primitive tube later undergoes a sort 
of S-shaped twist, and by a complex process of evolution 
develops into the heart. There are many modifications 
which may occur in the above-mentioned development, and 
some of these are recognized in the condition termed “con¬ 
genital heart.” The variability in the relation of the right 
and left vagus nerves to the sino-auricular node and the 
auriculo-ventricular bundle may, in part, be due to differ¬ 
ences in the evolution of the heart. There are several 
structures in the heart which possess particular significance 
as regards the fetal circulation. 

The Foramen Ovale is in the interauricular septum 
and is freely open until about the middle of fetal life, when 
a fold of tissue grows up from the posterior wall of the 
left auricle and acts as a valve in permitting the passage 
of blood only in the direction of right to left auricle. 

The Eustachian Valve is a fold of tissue projecting 
upward in front of the orifice of the inferior vena cava and 
tends to divert the blood from this vessel through the fora¬ 
men ovale into the left auricle. 

The Ductus Arteriosus (ductus Botalli) is a short 
tube, about 10 mm. in length at birth and 2 mm. in diameter. 
In fetal life it forms the continuation of the pulmonary 
artery, and opens into the aorta just beyond the origin of 


30 


MODERN CONCEPTION OF HEART DISEASE 


the left subclavian artery. It conducts the greater part 
of the right ventricular blood stream into the aorta. 

The upper and posterior part of the Interventric¬ 
ular Septum, which separates the aortic vestibule from 
the lower part of the right auricle and the upper part of 
the right ventricle, is derived from the inferior part of the 
aortic septum of the fetus. Owing to defective develop¬ 
ment of this septum, an abnormal communication may 
exist at this spot. 

Changes in the Circulation at Birth.— Soon after 
birth the development of the circulation in the lungs 
increases the pressure in the left auricle and the effect of 
this is to press the valve-like fold against the ring of the 
foramen ovale. The structures fuse and closure of the 
foramen is usually complete by about the tenth day. A 
further result of the onset of respiration is the diversion of 
the blood through the pulmonary arteries. The ductus 
arteriosus begins to contract and is usually completely 
closed by the fourth to the tenth day. Occasionally a 
small lumen persists. 

The changes in the circulation elsewhere in the body 
need not be described in this brief resume. 


CHAPTER II 
METHODS OF EXAMINATION 

Cardiac diagnosis is built up from the data collected by 
a variety of methods. Care and thoroughness are just 
as important in the diagnosis of heart as in other medical 
conditions. The physician who limits his examination to 
auscultation displays a lack of appreciation of the subject. 

History. —A careful general history should be ob¬ 
tained as a preliminary to one bearing more directly on 
the heart. The presence or absence of diseases known to 
cause heart affections is to be determined. Of special 
etiological importance are various infections, such as rheu¬ 
matic fever, chorea, tonsillitis, scarlet fever, pneumonia, 
puerperal sepsis, etc. If present, questions should be 
directed to develop the genuineness and severity of the 
above. A history of syphilis is always important. If the 
patient is said to have been treated in the past for cardiac 
disease, the details of this should be explored. 

The anamnesis should contain data as to the tolerance 
of exercise. A knowledge of the nature of the patient’s 
occupation, and whether it is pursued without symptoms, is 
often most useful. A statement as to the effect of climb¬ 
ing stairs and walking on the street is helpful in estimating 
the tolerance to physical exercise. In children, one may 
inquire if the patient can run and play games as well as 
other children. 

The nature and duration of symptoms, if any, should 
be noted. The more common of these are shortness of 
breath, cough, palpitation, pain, indigestion, undue fa- 

si 


32 


MODERN CONCEPTION OF HEART DISEASE 


tigue, etc. Sufficient details are indicated of any symp¬ 
toms that may be present. Thus, it is not enough to note 
that the symptom of palpitation is present, for intelligent 
questioning may at times produce a description of attacks 
of paroxysmal tachycardia. So-called nervous symp¬ 
toms should be duly recognized. 

Inspection. —The patient may present the mitral 
facies. Dyspnoea and cyanosis suggest some degree of 
heart failure. Visible pulsation of the carotid arteries, 
which is sometimes accompanied by a slight nodding or 
shaking of the head, points strongly to insufficiency of 
the aortic valve. Distention and visible pulsation of the 
external jugular veins is associated with engorgement of 
the right auricle. Exophthalmos and other signs of 
Graves’s disease should bring to the examiner’s mind the 
possibility of the heart in hyperthyroidism. 

Inspection should take note of the position and charac¬ 
ter of the apex impulse, if present. Any abnormal pulsa¬ 
tion or retraction requires explanation; depending on po¬ 
sition and character, they may point to an aneurism, en¬ 
largement of the right ventricle, adhesive pericarditis, etc. 
Bulging of the precordia is common in heart disease begin¬ 
ning in childhood. Clubbing of the fingertips may be 
associated with congenital heart disease and severe heart 
affections in early life. Epigastric pulsations may be due 
to an enlarged right heart, but as they occur in low-lying 
hearts, and rarely even in marked left ventricular hyper¬ 
trophy, the sign must be interpreted with caution. 

The legs may be obviously swollen from edema, and in 
the more marked cases the swelling may extend to the geni¬ 
tal region and trunk. As contrasted with edema of renal 
causation, that due to cardiac failure is more directly 


METHODS OF EXAMINATION 


33 


influenced by gravity. It should be remembered, however, 
that serious heart failure may be present without edema. 
The true reason for edema is obscure; that it is due solely 
to circulatory stasis, no longer seems a satisfactory expla¬ 
nation. Some chemical process has been suggested. 

Palpation. —The situation and extent of the apex 
beat, or point of maximum impulse, should be determined. 
In cases in which the apex beat is not palpable, it may 
become so if the patient is directed to lean forward to the 
left and to exhale fully. It is generally best to palpate 
with the tips of the fingers starting outside of the left 
border of the heart and proceeding inward. If the impulse 
is diffuse, the point of maximum forward thrust is to be 
taken as the apex beat. Its location is to be recorded 
laterally in relation to the midclavicular line (nipple line 
is about as accurate in male subjects) or other chest line, 
and vertically by the number of the thoracic interspace. 

It is suggested that in determining the number of the 
interspace, advantage be taken of the anatomical fact that 
the transverse ridge marking the junction between the 
manubrium and gladiolus of the sternum (often termed 
angle of Ludwig) is directly opposite the sternal articula¬ 
tion of the second rib. Starting with a finger placed above 
and another below this rib, by progressive straddling of the 
ribs downward, one can accurately determine the inter¬ 
space in which the apex beat presents. 

The position of the patient should be considered in 
drawing any conclusions from the location of the apex 
impulse. Thus, in the dorsal decubitus, the beat com¬ 
monly moves up one interspace from that of the sitting or 
standing position. The manoeuvre of palpating the im¬ 
pulse when the patient is lying on the left side is useful 


34 


MODERN CONCEPTION OF HEART DISEASE 


to bring out the mobility of the apex. An unduly wide 
swing to near the anterior axillary line or even further is 
often disclosed in hypertrophy of the left ventricle, but in 
this case the impulse in the axilla is really due to the lateral 
thrust of the wall and not of the apex of the enlarged 
ventricle. In some cases, where pericardial or pleuro¬ 
pericardial adhesions are present, the apex beat may re¬ 
main fixed. An abnormal position of the apex impulse 
may be produced by pleural effusions, ptosis of heart, and 
congenital or acquired dextrocardia. In insufficiency of 
the aortic valve, the apex impulse tends to be displaced 
downward and to the left, whereas in mitral stenosis the 
displacement, if present, is horizontal and to the left. 

The character of the cardiac impulse, best observed by 
palpation with the flat of the hand, may give further data 
as to the condition of the heart beneath. Thus if there 
is hypertrophy of the left ventricle, as in aortic regurgita¬ 
tion, the impulse feels heaving and sustained, while in many 
cases of mitral stenosis, the sensation is as though the chest 
wall were hit a sharp blow or tap which was as quickly 
withdrawn. 

The precordia should be palpated for the detection of 
any other pulsations and thrills. The loud purring thrill 
should be distinguished from the slight vibration, or “sug¬ 
gestion of a thrill,” which may be found in merely irri¬ 
table hearts. 

It is often necessary to combine auscultation with pal¬ 
pation in order to properly time pulsation and thrills. 
Thus an impulse over the body of the right ventricle may 
be found to be diastolic in time, with a systolic recession, 
and is good evidence of right ventricular enlargement. 
When this sign is present, it is the rule to find the apex 


METHODS OF EXAMINATION 


35 


impulse absent or poorly marked. Palpation of the ca¬ 
rotid pulsation in the neck is a reliable method of checking 
the time of the heart sounds. 

The hand placed over the second left costal cartilage 
may detect a forcible closure of the pulmonic valve. In 
mitral stenosis and in gallop rhythm there may be a double 
diastolic shock of the apex. Friction fremitus may be pal¬ 
pable in some cases of pericarditis. In interpreting an 
impulse near the head of the sternum as due to an aneurism 
or a dilated aorta, it should be remembered that when a 
deformity of the thorax and spine are present, a normal 
aorta may cause such an impulse, due to its abnormal 
position in close contact with the chest wall. Pulsation of 
the first part of the aorta may be palpated in the supra¬ 
sternal notch in case the aorta is elongated or dilated as in 
arteriosclerosis or aortitis, and also in patients in whom 
the vessels are merely atonic, or in whom the diaphragm is 
unduly high. 

Percussion. —The development of radiography has 
disclosed the limitations of percussion in determining the 
size and shape of the heart. In fact, some authorities go 
to the extreme of holding that percussion is valueless as 
a means of diagnosing the presence or absence of cardiac 
enlargement. With this opinion the writer is not in agree¬ 
ment. But it is desirable that the limitations of informa¬ 
tion obtained by means of percussion alone, should be more 
widely appreciated. A valuable contribution to this sub¬ 
ject was made in 1916, by G. C. Shattuck and others, at 
the Massachusetts General Hospital. 1 

Percussion that is of value is an art; it cannot be learned 

1 Shattuck, G. C.: Boston Med. and Surg. Jour., clxxiv:301 (March 
2, 1916), see also Internat. Clinics, iv, series 29:106, 1919. 




36 


MODERN CONCEPTION OF HEART DISEASE 


from books, but is acquired by experience from the clinical 
examination of patients, and its margin of error will be 
lessened if frequently checked by postmortem findings and 
especially by X-ray mensuration of the heart and aorta. 
It should be understood that skilled examiners may differ 
in the demarcation of a particular cardiac border, but that 
each may, as a result of experience in practicing percussion 
according to his own method, correctly determine the pres¬ 
ence or absence of enlargement of the heart. Since there 
is no normal-sized heart (the heart fits the patient and the 
shape of the thorax is subject to much variation) the 
measurements of the borders of cardiac dulness should 
always be recorded in relation to the chest lines. Thus the 
written statement that the left border of cardiac dulness 
extends to ‘TO cm. from the midsternal line” becomes 
informing to the reader, who may not have the patient 
available for personal examination, if there is added the 
relation to the midclavicular (nipple line is accurate enough 
in the male sex) or axillary lines, as “1 cm. outside the 
midclavicular line,” etc. The latter statement is more 
valuable than the former. 

Due allowance must be made for the difference in 
cardiac shape and location that is dependent upon the 
position of the patient. Thus the contour of the heart 
broadens and the organ assumes a higher level in the 
thorax when the patient changes from the standing or 
sitting to the horizontal posture. Still another factor that 
adds to the difficulty of accurately determining the size 
of the heart by percussion, is that the organ is subject to 
a rhythmic diminution and increase in magnitude coinci¬ 
dent with systole and diastole. This latter difficulty is 
met, in part at least, by repeating the percussion stroke and 


METHODS OF EXAMINATION 


37 


being guided by the average result. Both light and medi¬ 
um percussion are indicated, and the border of cardiac 
dulness is generally best appreciated if the percussion pro¬ 
ceeds from over the lung resonance toward the heart, 
rather than the reverse way. 

It should be appreciated that when the border of car¬ 
diac dulness extends around the curve of the chest wall, it 
is impossible for the percussion finding to agree exactly 


Lp' Lp. Lx. M. R. 



Fig. 4. —Comparison between percussion and teleradiography in the determination of the left 
cardiac border. R, right cardiac border ; M, midsteraal line; Lx, Lp, and Lp', the left cardiac border as 
determined by the X-ray, percussion with the measuring tape held horizontal, and when the latter is ap¬ 
plied around the curve of the chest, respectively. P, point on chest wall where left border of cardiac 
dulness begins. Diagram based upon a frozen section. 

with the measurement obtained by the Rbntgen examina¬ 
tion. The discrepancy is due to a simple problem of 
jffiysics which will be evident from a glance at the accom¬ 
panying diagram. (Fig. 4.) 

The right border of cardiac dulness is notoriously 
difficult to obtain. It demarcates the extension to the 
right of the right auricle, which, it should be remembered, 
lies at a level distinctly posterior to the chest wall. Also 
its proximity to the sternum introduces the factor of con¬ 
duction of the sound along that bone. 










38 


MODERN CONCEPTION OF HEART DISEASE 


To determine the curve of the left border of the deep 
cardiac dulness is often of value in physical examination. 
Normally it is convex inwards; a straightening or outward 
bowing of this line should suggest enlargement of the left 
auricle and the infundibulum, i.e., the part of the right 
ventricle adjacent to the origin of the pulmonary artery. 
The radiographer often reports somewhat as follows, “The 
heart is enlarged laterally, and is especially prominent in 
the region of the auricles. The picture is that of mitral 
stenosis.” This prominence of the left auricle can often 
be detected by percussion. The left auricle, of course, lies 
at a distinctly posterior level, and it is evident that an in¬ 
crease in the heart dulness to the left, at the level of the 
third and second intercostal spaces, is in part due to 
enlargement of the infundibulum. 

An increase in the area of absolute heart dulness may 
be found in enlargement of the right ventricle. 

Percussion outside the nipple, with the patient lying 
and turned towards the left side, will often bring out 
enlargement backward of the left ventricle. C. F. Hoover 2 
urges that percussion be performed with the patient sitting 
up and leaning forward, as then the heart is in better con¬ 
tact with the chest wall. 

Examination by percussion should always include the 
region over the great vessels. The "writer has found the 
bent-finger method of Plesch 3 of assistance in delimiting 
the extension to right and left of the supraeardiac dulness, 
in enlargement of the first part of the aorta. 

In the presence of pericarditis with effusion, percussion 

3 Hoover, C. F.: Jour. Amer. Med. Assn., 75, 24:1626 (Dec. 11, 1920). 

3 Brttgsch and Schittexhelm: Lehrbuch klinischer Untersuchungs- 
methoden, Urban and Schwarzenberg, Berlin and Vienna, 1911, p. 57. 



METHODS OF EXAMINATION 


39 


may disclose the heart dulness to be pear-shaped, with the 
small end towards the base of the heart. In large effu¬ 
sions, there may be an obliteration of the angle between the 
percussion line of the right auricle and the upper border 
of the liver. 

A knowledge of the anatomy of the heart and of the 
various shapes which the latter may assume, and an 
appreciation of the limitations of percussion, are most 
important in making valuable this method of examination. 

Auscultation. —Success in auscultation of the heart 
requires the use of a stethoscope equipped with both the 
diaphragm type of chest piece, such as is found in the 
Bowie’s stethoscope, and some sort of bell attachment. 
Most observers, and rightly so, acquire most of their skill 
with either the diaphragm or the bell-shaped chest piece, 
but they should be familiar with both, since experience has 
shown that there are murmurs which are better appreci¬ 
ated and at times only detected by one or the other attach¬ 
ment. Thus, the relatively high-pitched, diastolic murmur 
of aortic regurgitation is best heard when using the large 
diaphragm chest piece, while it often happens that it 
is necessary to change to the bell to detect the low-pitched 
apical diastolic murmurs of mitral stenosis. 

The late Austin Flint offered a reasonable explanation 
of the above in the following: “All elastic structures, how¬ 
ever, have their own vibration times, and when oscillations 
are transmitted to them at that rate they are set in motion. 
This is daily seen in the laboratory, when, as an ill-balanced 
centrifuge is gradually increased in speed, now one, and 
now r another pipette, rack, beaker, or burette begins to 
rattle, and subsides only when the centrifuge’s vibrations 
have altered to become more rapid. It is this which makes 
it necessary that marching troops break step while crossing 


40 


MODERN CONCEPTION OF HEART DISEASE 


bridges, and upon this same fundamental law depends the 
fact that, if the sound waves of one tuning fork reach a tun¬ 
ing fork, string, bell, or other sonorous body of similar 
pitch, the latter is set in action. This lav/ is made of prac¬ 
tical use in analyzing sounds composed of several tones, by 
exposing a series of resonators to the compound vibration 
and noting which resonators are set in covibration. It is 
also of great importance in the construction of stethoscope 
bells. When dealing with faint murmurs of low pitch, the 
old Gannet type of stethoscope not infrequently settled an 
argument, because the large resonating cavity of its bell 
intensified murmurs of that pitch.” 4 

Direct auscultation is performed by applying the ear 
of the observer direct to the patient’s chest. For esthetic 
reasons a thin towel or handkerchief may be employed to 
prevent actual contact with the patient’s skin. This 
method of auscultation is especially useful in the detection 
of aortic murmurs and is most frequently resorted to by 
those who do not use the large diaphragm attachment to 
their stethoscope. 

After noting the general character of the sounds, the 
rhythm, etc., it is commonly necessary that the auscultator 
should concentrate his attention on individual sounds or 
murmurs, excluding for the moment the other auscultatory 
phenomena (a trick that can readily be learned). It is 
essential to time the sounds in relation to the heart cycle. 
In most instances this may be judged correctly by the 
character of the sounds, but it is a good rule to always 
obtain confirmation by inspection or palpation of the apex 
or carotid pulsation. To the beginner, it is suggested that 
he consciously direct his attention to noting the intensity, 

4 A Manual of Physical Diagnosis, by Austin Flint, eighth edition, revised 
by H. C. Thatcher. Lea & Febiger, 1920, p. 22. 



METHODS OF EXAMINATION 


41 


duration, point of maximum intensity, range of trans¬ 
mission, etc., of each sound or murmur. With experience, 
much of this becomes subconscious. 

No auscultation may be said to be complete unless the 
patient is examined both while in the sitting or standing 
position and also in the horizontal posture. The position 
of the patient influences the contact of the heart with the 
chest wall and therefore has a direct bearing on the trans¬ 
mission of the various murmurs. In the main, basal mur¬ 
murs are of maximum audibility when the patient inclines 
his chest well forward, while the apical bruits are better 
appreciated when the patient is lying on the back or lying 
turned obliquely toward the left. Further emphasis will 
be laid on these points in the discussion of the various 
valve lesions. 

The effect of exercise on the auscultatory phenomena 
should always be noted. An acceleration of the heart rate, 
as a result of exercise, may cause an irregular rhythm to 
be displaced by one that is regular, and serves to rule out 
auricular fibrillation. Exercise, by increasing the veloc¬ 
ity of the flow of the blood through the heart, may enable 
the examiner to hear certain murmurs, or may so increase 
the audibility of some suspicious sound, that a decision can 
be made with confidence as to whether it is a murmur 
or not. 

The inhalation of the fumes of a pearl of amyl nitrate 
appears to act very similarly to exercise in its effect on the 
heart sounds and murmurs. To the writer it appears to 
offer no particular advantage. 

Accuracy in auscultation, of course, requires experi¬ 
ence. At least average acuteness of hearing is necessary. 
It would seem that the two greatest contributors to a sue- 


42 


MODERN CONCEPTION OF HEART DISEASE 


cessful result are, first, the ability to analyze the findings 
present by the concentrating of the examiner’s attention 
on the sounds heard with one phase of the heart cycle at a 
time; and, second, the deliberate directing of his mind 
toward the detection of the auscultatory phenomena, 
whose possible presence is suggested by a clear-cut knowl¬ 
edge of heart affections. 

Blood Pressure Determination. —This is usually 
accomplished by the auscultatory method, using a pressure 
cuff over the brachial artery and placing the end of the 
stethoscope over the vessel, just distal to the bandage 
wrapped around the arm. Sufficient instructions are fur¬ 
nished by the instrument makers. The aneroid type 
is nearly as accurate as that in which a column of mer¬ 
cury is employed, and for all clinical purposes either type 
is suitable. 

The sounds heard in the auscultatory method, when the 
pressure in the cuff is allowed to fall gradually, may be 
divided into five phases: (1) the sudden appearance of a 

clear sound, (2) acquisition of a murmurish quality, 
(3) replacement of the murmur by a sound which becomes 
progressively louder, (4) muffling of the sound, (5) dis¬ 
appearance of the sound. The first phase is generally 
taken as the systolic pressure and the fifth as the diastolic 
level, the difference between them being the pulse pressure. 
When the Corrigan type of pulse is present, sometimes all 
sound may not disappear. In that case it is necessary 
to use the fourth phase, which is estimated to be about 
5 to 6 mm. higher. 

In the palpatory method, the arm band is applied 
as above and the reading is taken the moment the finger 
detects the return of the pulse in the radial artery as the 


METHODS OF EXAMINATION 


43 


pressure in the cuff is allowed to fall. In this method the 
reading averages 5 to 10 mm. of mercury lower than in the 
auscultatory method. The diastolic pressure cannot be 
obtained by palpation. Both in health and in association 
with aortic regurgitation, the systolic may be higher and 
the diastolic lower in the femoral than in the brachial 
artery. Starling 5 explains this as due to the summation 
of waves reflected from the periphery. The femoral artery 
is larger, its walls are more rigid and the peripheral resist¬ 
ance is more localized; all of these contribute to make the 
reflected waves greater. 

The blood pressure is much influenced by psychic and 
mechanical conditions. A single reading is of but limited 
value, as there is too great a chance that the result may 
not represent the usual or average pressure level in the 
patient under examination. The test should be repeated 
on several occasions under as nearly the same conditions 
as possible. Care should be taken to avoid exposure to 
cold, and the physical and mental relaxation of the patient 
should be sought. Except under the most carefully con¬ 
trolled conditions and when readings are taken over a 
period of twenty minutes or more, the figures should be 
regarded as mere approximations. The hemodynamics of 
blood pressure are too subtle to be considered in an off¬ 
hand manner. 

Exercise Tolerance. —An estimate of the response 
to exercise or, as it is commonly termed, the exercise toler¬ 
ance, is essential in forming an accurate opinion of the 
heart which is under examination. Many procedures have 
been proposed in the endeavor to obtain a scientific estimate 
of the cardiac efficiency, but since, in the author’s opinion, 

* Stabli;ng, E. H.: Principles of Human Physiology, 3rd edit, 1920. Lea 
and Febiger, p. 971. 




44 MODERN CONCEPTION OF HEART DISEASE 

their value is doubtful or as yet unsettled, they will not 
be described . 0 

It is not rare to find individuals who can satisfactorily 
perform some set test, such as lifting a pair of dumbbells 
fifty times, but yet cannot perform their daily tasks without 
circulatory symptoms. Nervous factors frequently inter¬ 
fere with the reliability of tests carried out in the physi¬ 
cian’s office. Of course, since patients differ so widely in 
age, weight, stature, sex, and habituation to physical 
effort, it is impracticable to use the same exercise for all. 
It seems sounder to subject each case to some physical 
effort suitable to the individual (an obese, middle-aged 
woman should hardly be asked to bend forward until the 
finger tips touch the floor, while the knees remain unflexed) 
and which will cause a definite elevation of the heart rate. 
And then one should carefully watch for effects such as 
breathlessness, cyanosis, undue elevation of the heart rate, 
etc., which are untoward for the individual under examina¬ 
tion. It follows, then, from the above statements, that 
the estimation of the exercise tolerance remains a matter 
of the physician’s judgment and not a clinical fact like the 
blood count. Any attempt to resort to a numerical basis 
appears to the writer to be fallacious unless controlled by 
a clear knowledge of its limitations and its physiological 
background. It should be remembered that exercise, if 
pushed far enough in a person with a normal heart, will 
cause symptoms and signs similar to those produced in a 
patient with some degree of cardiac failure. Experience 
is the best guide in judging when the effects of exercise 
may be said to be untoward. 

The information of greatest value in forming an esti- 

9 A letter by C. W. Crampton in the Jour. Amer. Med. Assn., 76, 16: 1121 
(April 16, 1921), contains references to pertinent articles on this subject. 




METHODS OF EXAMINATION 


45 


mate of a patient’s heart is whether it permits him to carry 
on his daily work without symptoms. Any diminution in 
the capacity to perform work to which the patient has been 
habituated requires explanation. Questioning as to the 
effect of ascending stairs or walking on the street often 
elicits helpful information. 

The exercise tolerance should rarely be tested in the 
presence of fever and it is unnecessary in the presence of 
definite evidence of cardiac failure. It should be reserved 
for cases in which some doubt exists as to the presence of 
cardiac disease, or as an important aid to assessing the 
amount of impairment of the heart, and a useful guide 
to treatment. 

Thomas Lewis, 7 in his usual lucid manner, summarizes 
the interpretation to be placed upon a deficiency in the 
exercise tolerance somewhat as follows:— 

1. In the presence of definite enlargement of the heart, 
aortic disease, mitral stenosis, or fibrillation of the auricles, 
any undue distress after exercise should be attributed to 
cardiac disease. 

2. In young subjects, if none of the above four condi¬ 
tions are present, a deficient exercise tolerance should 
rarely be attributed to the heart. Tuberculosis and other 
pyogenic infections are likely. 

3. In the elderly, in whom there is no sign of structural 
change, if the exercise tolerance is poor, the heart should be 
blamed. Such persons are liable to suffer from angina 
pectoris or myocardial damage, in which the chief symp¬ 
toms may be breathlessness or undue fatigue, rather 
than pain. 

7 “Cardinal Principles in Cardiological Practice,” Brit. Med. Jour., 2:621 
(Nov. 15, 1919). 



46 


MODERN CONCEPTION OF HEART DISEASE 


Rontgen Examination. —This is primarily the prov¬ 
ince of the radiologist and, therefore, its discussion will 
be limited to some of the points thereon. The Rontgen 
findings are particularly useful in giving us the most accu¬ 
rate data as to the shape and size of the heart and aorta, 
and to the detection of aneurisms, etc. 

The patient should first be examined under the fluoro- 
scope and the general contour of the heart and great vessels 
observed. Any abnormal pulsations should be noted, and, 
with experience, considerable can be concluded as to the 
heart rhythm by watching the contractions of that viscus. 
Examination with the patient standing at oblique angles 
should not be omitted, as without this procedure, certain 
aneurismal changes of the aorta may escape detection. 

One or more exposures are then taken, and the nega¬ 
tives studied for details. These are usually taken at a 
distance sufficient to permit mensuration of the heart and 
aorta. Seven feet is the standard distance in many clinics, 
but it can be shown that the margin of error at a four-foot 
distance is small. In other words, it is possible to study 
the size of the heart in plates taken at a distance of four or 
more feet; below this distance the possible distortion in 
the size of the image is too great. 

Tables of the measurements of hearts in normal men 
have been published by several radiologists, but these have 
failed to be of the value that was hoped. The difficulty is 
that there is no normal-sized heart; the heart fits the indi¬ 
vidual in whom it is placed. The variations in the different 
measurements amount to several centimetres. Of late 
there has been an attempt to use the ratio of the transverse 
diameter of the heart to the internal transverse diameter 
of the chest. Danzer 8 found this ratio to vary in the 


8 Danzer, C. S.: Amer. Jour. Med. Sci., 157: 520, 1919. 




METHODS OF EXAMINATION 


47 


normal from 39 to 50 per cent. If the ratio was 53 per 
cent, or higher, the heart was definitely pathological. 
Even when the ratio does not exceed 50 per cent., cardiac 
hypertrophy cannot be ruled out; for example, in the drop 
heart of ptosis, judgment must be guided by the in¬ 
trinsic measurements. 

The orthodiagraphic method of determining the size of 
the heart is complicated, but offers some advantage over 
the method, teleradiography, discussed above. Its de¬ 
scription will be omitted. 

The contour of the heart, as shown on the Rontgen 
film, often enables the radiologist to make a correct diag¬ 
nosis of the existence of valve lesions. Thus, when he 
writes, “The heart is enlarged transversely, and is particu¬ 
larly prominent in the region of the auricles,” he is likely 
to add, “The picture is that of mitral stenosis.” Hyper¬ 
trophy of the left ventricle is recognized by extension of 
the shadow downward and to the left. 

The shadow of the great vessels may be enlarged or 
abnormal in contour. Broadening may be due to syphilis, 
arteriosclerosis, hypertension, rheumatic heart disease, high 
diaphragm, or even a dilated pulmonary artery. These 
conditions should be remembered before deciding, on 
Rontgen evidence alone, that an increase in width of the 
shadow of the great vessels is sure evidence of luetic infec¬ 
tion of the aorta. This matter and the occurrence of aneu¬ 
risms will be dwelt upon further in subsequent chapters. 

Vital Capacity. —This is determined by measuring 
the volume of air which is expressed in a forced expiration. 
The patient exhales the maximal amount of which he is 
capable, into a spirometer, and the content of air is read 
from the scale on the instrument. 

The actual value of the method is gradually being 


48 


MODERN CONCEPTION OF HEART DISEASE 


established. Occasionally there is an evident lack of co¬ 
operation on the part of the patient. A decrease of the 
vital capacity may be due to other causes than heart dis¬ 
ease, for instance, pulmonary affections. An authority 
on this method of examination well expresses its present 
status as follows: “In heart disease the vital capacity is 
of practical value after the diagnosis has been established 
and as a direct index of cardiac reserve.. . The actual 
change in any given case is of more importance than the 
change in percentage of vital capacity as compared with 
normal standards. In general, physical training may 
increase the vital capacity about 25 per cent, above the 
normal, and extreme physical weakness may reduce the 
vital capacity about 25 per cent, below the normal 
standards.” 9 

The chief reliable signs of heart disease have been 
listed by Lewis, 10 as follows: 

(a) An aortic diastolic murmur. 

(b) Distinct over-distention of the veins of the neck. 

(c) Definite signs of enlargement of the heart. 

(d) An irregular heart action which is maintained on 

exercise (the heart rate being high). 

(e) A diastolic rumble at the apex. 

(f) A basal or apical thrill. The thrill must be an 

unmistakable “purr;” a suspicion of thrill is 
insufficient. 

(g) Widespread arterial disease or a persistent blood 

pressure, 180 or over in an elderly man, arterial 
disease or a persistent blood pressure of 160 
or over in a young man. 

“Peabody, F. W.: Med. Clin. No. Amer., 4, 6: 1655 (May, 1921). 

10 Lewis, T.: The Soldier’s Heart and the Effort Syndrome, 1919, Paul 
B. Hoeber, New York, p. 132. 



CHAPTER III 


METHODS OF EXAMINATION (cont.) 

Graphic Methods 

The graphic methods are the examinations with the 
polygraph and the electrocardiograph. The use of these 
instruments of precision has already become a valuable 
addition to clinical cardiology. They will be described in 
order. The reader may prefer to defer reading these 
chapters until reaching the section on Functional Con¬ 
ditions. Without their assistance, however, it is doubtful 
if the various arrhythmias will be clearly understood. 

POLYGRAPHIC EXAMINATION 

The brilliant studies of the venous pulse by James 
Mackenzie, supplemented by those of Wenkebach and 
others, have made possible the understanding of many 
cardiac conditions hitherto obscure. The taking of pulse 
tracings is now widely practised. Besides its value in 
diagnosis, a polygram serves as a permanent record of 
certain conditions which at best can be but imperfectly 
described by words. The information obtained is some¬ 
what less than that produced by electrocardiography, save 
in the matter of pulsus alternans, which is best demon¬ 
strated by a tracing of the arterial pulse. The polygraph 
possesses the additional advantage that it may readily be 
carried to the patient’s bedside and thus used when an 
electrocardiographic examination is unobtainable. 

There are several sphygmographs and polygraphs to 
choose from, but perhaps the best known, in this country, 
are the Mackenzie ink polygraph and the Sanborn instru- 

4 49 


50 


MODERN CONCEPTION OF HEART DISEASE 


ment. Both of these polygraphs (many writings) permit 
the simultaneous recording of any two pulsations. The 
tracings are registered by pens writing in ink on a strip of 
paper fed at chosen speeds by a clockwork mechanism. 
A third pen records the time in fifths of a second. De¬ 
tailed description of these instruments will be omitted; 
prospective owners will find sufficient information in the 
descriptive leaflets supplied by the manufacturers. 

It must not be thought that clinical polygraphs repro¬ 
duce accurately the course of events inside the vessel under 
examination. Their vibration frequency is not great 
enough , 1 and, on account of their weight, the writing pens 
tend to override the mark. This results in an exaggeration 
of the height of the waves and often causes purely artificial 
secondary oscillations on the downstroke. Only the ma¬ 
jor waves are recorded, and these are given unnaturally 
rounded outlines, while the finer waves are slurred over 
or combined . 2 Too great friction of the pens against the 
paper introduces further mechanical defects. In spite of 
these limitations the pulse tracings are of value, due to the 
system of interpretation by means of the time relations 
between the arterial and venous curves, so extensively 
developed by Mackenzie, Wenkebach and others. 

The taking of pulse tracings is a most fascinating study, 
but will prove disappointing unless the instrument is kept 
in good condition, especially as regards the renewal of the 
rubber of the tambours. Care and the use of much pa¬ 
tience are often needed. The tracings are of uncertain 
value unless the examiner acquires a knowledge of their 

1 Wiggers, C. J.: Circulation in Health and Disease, Lea and Febiger, 

Philadelphia and New York, 1915, p. 109. 

2 Lewis, T.: The Mechanism and Graphic Registration of the Heart Beat, 
Paul B. Hoeber, New York, 1920, p. 21. 



METHODS OF EXAMINATION 


51 


interpretation. Such knowledge may be obtained from 
the literature and by personal instruction. If approached 
in this manner the polygraph will become an instrument 
affording considerable pleasure and information pertain¬ 
ing to the heart, and will not be discarded after a few weeks. 

The arterial curves are obtained by applying the receiv¬ 
ing apparatus over the radial or brachial artery and adjust¬ 
ing until the writing pen registers the maximum excursion. 
If the pulse is of very small volume it may be recorded 
with difficulty. 

In taking a tracing from the jugular vein it is usually 
essential that the patient be lying flat or nearly so, as other¬ 
wise the “a” or auricular wave may not appear at the neck. 
The cup is usually applied over the jugular bulb which lies 
beneath the angle between the clavicle and the posterior 
border of the sterno-mastoid muscle and the pressure ad¬ 
justed until the optimal record of the waves is obtained. 
At times the cup must be moved to adjacent positions; 
in some cases a more satisfactory tracing may be obtained 
from the external jugular vein where it courses more pos¬ 
teriorly in the neck. The presence of severe dyspnoea with 
marked inspiratory retraction of the cervical tissues is an 
obstacle to the recording of a successful venous curve. 

In nervous children or in patients who, because of 
delirium or some other reason, will not keep quiet, it may 
be a waste of time to attempt to use the polygraph. 

The limitations set for this book make it possible to 
present but an outline of the study of pulse tracings. 
Those interested in further details of polygraphy should 
consult the literature . 3 

8 One of the more recent books is, Graphic Methods in Heart Disease, 
by Hat, John; Oxford Medical Publications, London, 1921. 



52 MODERN CONCEPTION OF HEART DISEASE 
ARTERIAL PULSE TRACING 

The arterial pulse curve, or sphygmogram, is used for 
the detection of pulsus alternans, the study of respiratory 
variations in volume, and in combination with the venous 
curve forms the polygram. Study of the arterial tracing 
often permits identification of the type of disordered heart 
action; the proof, however, usually requires the polygram 
or electrocardiogram. 

Pulsus Alternans is shown by a sphygmogram in 
which large and small waves alternate; the waves must be 
evenly spaced or the small waves may show slight delay, 
that is, in the tracing the small wave is further from the 
larger wave that precedes than from the one that follows 
it. The electrocardiogram and other evidence have shown 
that the contractions of the heart occur at equal intervals 
of time; the delay of the small wave is due to the fact that 
with the smaller output of blood there is a delay in the 
rise of aortic pressure and in the registration of the pulse 
wave. True pulsus alternans is to be distinguished from 
certain types of bigeminal pulse, due to the occurrence of 
an extrasystole after every normal beat, by the fact that 
in this pseudo-alternation, the longer pause follows the 
smaller wave, i.e., the latter is premature. 

Pulsus alternans is usually more prominent and some¬ 
times detected only in the beats immediately following an 
extrasystole or a slight increase in the ventricular rate. 
Alternation is common in the accelerated pulse beats of 
paroxysmal tachycardia or flutter. 

Respiratory Variation in the strength of the arterial 
pulse waves is indicated where this occurs synchronous with 
the phases of respiration. For absolute proof, a respira- 



Fig. 5. —Upper tracing. Pulsus alternans. Lower tracing. Ventricular premature beats causing 
pseudo-alternation of the pulse. The small waves, which indicate the extrasystoles, are nearer to the pre¬ 
ceding large waves. The paper is travelling at a more rapid rate than in the tracing of pulsus alternans. 
(The interpretation of these and the succeeding polygrams has been checked by electrocardiograms.) 



Fig. 6.—Normal polygram. 




Fig. 7.—Sinus arrhythmia. Note alternate acceleration and slowing of the pulse. 




























METHODS OF EXAMINATION 


53 


tory tracing, or pneumogram, should be taken simultane¬ 
ously. A respiratory variation in the pulse volume is 
often associated with the alternate acceleration and slowing 
of the pulse rate that occurs in sinus arrhythmia. Inspira¬ 
tory weakening in the volume of the pulse is often termed 
pulsus paradoxus, or Kussmaul’s pulse; while it may 
be present in adherent pericarditis, it has been repeat¬ 
edly demonstrated that it may be without pathological 
significance. 

Dominant Rhythm. —The first step in the analysis of 
tracings of an irregular arterial pulse is to determine the 
presence or absence of a dominant rhythm. The latter 
may be defined as a rhythm which governs more or less the 
contractions of the ventricle. Usually the dominant 
rhythm arises in the sino-auricular node, but occasionally 
in some other part of the heart. 

In an arteriogram of an irregular pulse, those waves 
which are preceded by the longest pauses and are greatest 
in amplitude are usually initiated by the dominant rhythm. 
A run of four or more regular beats, if these are the most 
forcible seen, reveals the presence of a dominant rhythm. 
The latter is displayed if the phases of irregularity are 
repeated, however irregular such phases may be; the pres¬ 
ence of a controlling rhythm may be assumed whenever 
an irregular pulse shows periodicity of any kind . 4 When 
the dominant rhythm is undisturbed, a pulse irregularity is 
due to heart-block or extrasystoles arising in the ventricles . 5 

The determination of a dominant rhythm in an irregu¬ 
lar arterial pulse is of importance in excluding an arrhyth- 

1 Lewis, T.: The Mechanism and Graphic Registration of the Heart Beat, 

p. 134. 

8 Exceptionally in the auricle. 



54 


MODERN CONCEPTION OF HEART DISEASE 


mia due to fibrillation of the auricles. Since the 
identification of the different types of arrhythmia is 
greatly facilitated by the addition of data from the simul¬ 
taneously recorded phlebogram, and this is readily avail¬ 
able by the use of the polygraph, discussion of the subject 
may perhaps be more profitably continued if the evidence 
from the venous tracing is combined with that from 
the arterial. 

VENOUS CURVES 

Tracings from the jugular vein present a succession 
of peaks and summits often arranged in a bewildering 
fashion. The curves are so variable that their interpreta¬ 
tion should not be attempted without reference to an 
accompanying arteriogram. A number of waves may 
be present. 

Abscissae or index marks should be present in both the 
venous and arterial curves. They are lines in the tracing 
made by stopping the clockwork of the polygraph and 
allowing the pens to inscribe an upright line on the paper 
while stationary. 

The “C” Wave 6 represents the onset of ventricular 
systole. It may be identified by measuring the distance 
from any radial upstroke to an abscissa and transferring 
the measurement to the venous curve after correcting for 
the time required for transmission from the level of the 
neck to the wrist. If the arterial curve is obtained from 
the radial artery it has been shown that a correction of 0.1 
second is needed, while if it is from the brachial artery, 
as is usual with the Sanborn polygraph, the correction is 

6 An excellent description of the fundamentals of the venous pulse will 
be found in “The Venous Pulse,” Ewing, E. M.: Amer. Jour. Physiol., 
xxxiii:158, 1914. 




METHODS OF EXAMINATION 


55 


nearer one half as much, or 0.05 second. The distance to 
be allowed for this correction is determined by comparison 
with the intervals inscribed by the time marker. The latter 
records periods of 0.2 second and therefore the correction 
is one half or one quarter of these spaces, according as 
the arterial tracing is from the radial or brachial artery, 
respectively. As the “c” in the neck occurs earlier than 
the arterial upstroke, the correction should be added to 
the arterial measurement if the latter is taken to the left 
of an abscissa ( i.e ., the abscissa being on the right) and 
subtracted if the measurement is obtained from the right 
side of an abscissa. 

A convenient method of identifying a series of “c” 
waves is to mark a series of radial or brachial upstrokes 
and the adjacent abscissa on the edge of a strip of paper. 
The latter is then transferred to the venous curve and 
moved to the left or right of the corresponding abscissa 
according to the correction (described above) that is 
needed. The marks will then underlie the beginning of 
the “c” waves. The “c” or carotid wave is so called as it 
was thought to be due to the impact of the carotid artery, 
and while in the neck it is synchronous or nearly so with 
the carotid pulsation, it has been shown to be present in 
the vein proximal to the beginning of the carotid artery. 

The “V” Wave. —The end of ventricular systole is 
represented in the jugular curve by the apex of the “v” 
or ventricular wave, which is probably due to stasis. The 
“v” wave is synchronous with the bottom of the dicrotic 
notch in the radial tracing. It may be identified by trans¬ 
ferring to the venous tracing the measurement between 
the abscissa and bottom of the dicrotic notch in the arterio- 
In insensitive curves the dicrotic notch may not be 


gram. 


56 


MODERN CONCEPTION OF HEART DISEASE 


well represented, and in this case experience has shown that 
a sufficiently close estimate of its position may be made 
about two-fifths of a second after the “c” wave; absolute 
accuracy is not needed for this point. If desired a strip 
of curves from the carotid artery may be taken and the 
length of a beat transferred to the jugular tracing. Care 
should be used not to mistake a notch immediately follow¬ 
ing, in some tracings, the arterial upstroke for the dicrotic 
notch; it is earlier than the latter and is an artifact due to 
overshooting of the pen. 

It is important to determine the “v” waves in poly¬ 
grams; they may be mistaken for the “a” waves, or may 
coincide with the latter, in which case an exaggerated 
wave usually results. The “v” wave may be notched 
or insignificant. 

The “A” Wave. —The auricular wave is found directly 
before the upstroke of “c,” and represents the auricular 
contraction in the venous curve. Normallv it should be 
about 0.2 second before the onset of the carotid wave. 
A series of equidistant waves located in the diastolic phases 
of the phlebogram are usually “a” waves. If the wave 
preceding the “c” wave is prominent, it is the more certain 
to be the true auricular wave. When identification of 
“a” is dubious further evidence should be obtained from 
a tracing of the cardiac apex or from the electrocardio¬ 
gram. According to Lewis, 7 “It is a golden rule to accept 
only those curves in which the interpretation is transparent, 
or in which repetitions in detail are secured.” 

The “H” or “B” Wave. —This wave is found in early 
diastole in some venous tracings of a slow rhythm. It 

7 Lewis, T.: The Mechanism and Graphic Registration of the Heart Beat, 
p. 142. 



METHODS OF EXAMINATION 


57 


occurs synchronous with or a little after the third heart 
sound. Clinically it is unimportant. 

The A-C Interval. —This is the period between the 
upstrokes of the corresponding waves. It is used as an 
index of the auriculo-ventricular conduction period, though 
it is usually longer (not more than 0.1 second) than the 
P-R interval of the electrocardiogram. Normally the a-c 
interval varies from 0.1 to 0.2 second; a lengthening to 0.3 
second or more indicates defective conduction between the 
auricle and ventricle. 

The Ventricular Form of Venous Pulse is repre¬ 
sented by the absence of distinct “a” waves and the occur¬ 
rence of the chief summits within the limits of ventricular 
systole: the Auricular Form of Venous Pulse is char¬ 
acterized by the presence of the “a” waves in addition to 
those associated with the contraction of the ventricle. 
Care must be taken that the absence of the “a” wave is not 
due to an error in the technic of taking the tracing from 
the neck. Thus the auricular wave will often not be 
recorded unless the patient is lying approximately hori¬ 
zontal, or if the receiving cup is placed over the carotid 
artery rather than in the positions described above. If 
the heart rhythm is regular, the ventricular form of venous 
pulse may be due to engorgement of the auricle, simultane¬ 
ous contraction of auricle and ventricle, or regular action 
of the ventricle with auricular fibrillation. The ventric¬ 
ular form of venous pulse, associated with an irregular 
rhythm of the heart, is evidence of auricular fibrillation. 

Sinus Arrhythmia. —The polygram shows that all 
waves are present and in normal relation to each other, 
but they display a rhythmic acceleration and slowing. The 
change in rate usually corresponds to the phases of respira- 


58 


MODERN CONCEPTION OF HEART DISEASE 


tion. Variation in volume is also often present, as already 
mentioned in the discussion of the arteriogram. A less fre¬ 
quent form is the so-called phasic type of sinus arrhythmia, 
in which the acceleration or slowing persists for a longer 
period than that of inspiration or expiration. 

Sino- auricular Block. —This relatively infrequent 
arrhythmia is less readily recognized in the polygram. An 
apparently normal tracing in which the frequency of the 
waves is suddenly reduced to half, or approximately half, 
is a common form. At times a single beat may be dropped, 
as in some cases of auriculo-ventricular heart-block, but 
distinguished from the latter by the fact that the “a” wave 
disappears as well as the “c” and “v” excursions. 

Premature Bex^ts or Extrasystoles may arise in the 
auricle or in the ventricle, and exceptionally in the A-V 
node. In the auricular type the ventricular waves (“c” 
and “v”) are preceded by an “a” wave in the venous curve, 
while in the ventricular type the “a” is absent. The pre¬ 
mature beat may or may not appear in the arterial tracing 
according as the heart expels an amount of blood sufficient 
to make a wave in the artery. If the “a” wave of the 
premature auricular beat happens to coincide with the “v” 
or “c” excursions of the ventricular contraction in response 
to the previous auricular systole, a wave of exaggerated 
height occurs due to the superimposition of the two waves. 
A further explanation of these amplified waves is that the 
force of auricular systole is felt more strongly in the jugu¬ 
lar vein when the auricle contracts against a closed auriculo- 
ventricular valve. 

Premature beats are almost always 8 followed by a 
pause, and by noting the length of the latter it is often 


8 Interpolated extrasystoles are a rare exception. 





Fig. 8.—Auricular premature beats. 


s 







Fig. 9.—Ventricular premature beat. 



Fig. 10.—Paroxysmal tachycardia of auricular origin. The paroxysm has a duration of but ten 
beats, an auricular premature beat is recorded in the first part of the tracing,.and the rapid rhythm is 
followed by the characteristic post-paroxysmal pause. (After Sir Thomas Lewis.) 





















Pig. 11. Auricular Bbrillation. Lower tracing taken at a greater speed of the paper. Some ff waves are marked. 














METHODS OF EXAMINATION 


59 


possible to determine the origin of the beat. The pause 
following the ventricular extrasystole is always fully com¬ 
pensatory, i.e., of such a length that the succeeding beat of 
the normal rhythm occurs at exactly the time it would be 
expected if no extrasystole had occurred, and the dominant 
rhythm is not disturbed. When the pause is compensatory 
it will be found that the cycle of the premature beat and its 
succeeding pause is just equal to the sum of two normal 
heart cycles. The pause following a premature beat of 
auricular origin varies; it is usually longer than that after 
the normal beats and less than fully compensatory, but 
it may be equal to the normal pause, and rarely it may even 
have a duration that is fully compensatory. The varia¬ 
tion in the post-extrasystolic pause is dependent on the 
distance of the new impulse centre from the sino-auricular 
node, from which the dominant rhythm starts, and the 
amount of the prematurity of the extrasystole. In the 
case of auricular extrasystoles followed, as is nearly always 
true, by a less than compensatory pause, the succeeding 
beat comes before it would have come if the premature beat 
had not occurred and the dominant rhythm is disturbed. 
In brief then, if the extrasystole disturbs the dominant 
rhythm it may confidently be ascribed to the auricle, where¬ 
as, if there is a compensatory pause so that the dominant 
rhythm is not disturbed the origin of the extrasystole is 
usually ventricular, but it may exceptionally be auricular. 

The nodal extrasystole is not common. It gives rise 
to an exaggerated wave in the phlebogram due to the si¬ 
multaneous contraction of the auricle and ventricle; the suc¬ 
ceeding pause is usually compensatory. Extrasystoles 
originating in the A-V node are much more clearly identi¬ 
fied in the electrocardiogram. 


60 


MODERN CONCEPTION OF HEART DISEASE 


In cases of complete auriculo-ventricular heart-block, 
in which the ventricle is beating in response to an impulse 
centre in its own tissues, ventricular extrasystoles may 
occur and they interrupt this dominant rhythm exactly 
as auricular premature beats do the rhythm from the sino- 
auricular node. This combination is, however, of infre¬ 
quent occurrence. 

Interpolated extrasystoles are ventricular contractions 
which occur prematurely and in which the retrograde prog¬ 
ress of the impulse to the auricle is blocked in the auriculo- 
ventricular bundle. In this case the rhythm of the auricle 
is undisturbed; the ventricle also contracts in response to 
each auricular impulse. The interpolated ventricular 
contraction may be said to be the only extrasystole which 
is literally an extrasystole. It is not common. 

Paroxysmal Tachycardia. —The arteriogram shows 
a series of rapid and regular beats which may be so close 
together that the succeeding beat starts on part of the 
dicrotic wave and gives an anacrotic effect. In the jugu¬ 
lar curve the “a” wave may coincide with part of the pre¬ 
ceding ventricular systole and cause the wave to be 
superimposed. In this manner the ventricular form of 
venous curve may result. It is frequently not possible 
to determine from the polygram whether the tachycardia 
originates in the auricle or in the ventricle unless the trac¬ 
ing shows the onset or cessation of the paroxysm. In that 
case it is usually possible to identify and establish the origin 
of a premature beat which initiates the attack and may 
often be seen at its termination. Alternation of the arte¬ 
rial waves is common in paroxysmal tachycardia. At 
times it is difficult to obtain satisfactory polygraph trac¬ 
ings due to the small volume of the pulse. 


METHODS OF EXAMINATION 61 

Auricular Flutter. —In this condition the auricular 
rate averages about 300 per minute and the waves in the 
venous pulse are often too feeble to be recorded, in other 
cases it is difficult to disentangle them from the ventricular 
waves, and at times the phlebogram may closely simulate a 
normal jugular tracing. 9 The arteriogram may be regu¬ 
lar or irregular; in the latter case it can be established that 
a dominant rhythm is present. The signs of a dominant 
rhythm have been discussed above, but the method of 
spacing, by which the irregular arterial tracing of flutter 
is interpreted in relation to the auricular rhythm, is com¬ 
plicated and cannot be clearly presented in the limits set 
for this chapter. The interested reader is referred to the 
larger books of Lewis 9 and others. The diagnosis of auric¬ 
ular flutter usually requires confirmation by the electro¬ 
cardiogram, and in this, fortunately, the evidence is nearly 
always clear. 

Auricular Fibrillation. —In the arterial tracing the 
picture of absolute arrhythmia is presented; a dominant 
rhythm is absent. The venous curve discloses the absence 
of the “a” waves, i.e., it is the ventricular form of venous 
pulse. In the cases of long standing in which considerable 
dilatation of the auricle is present the venous curve shows 
an ascent during the longer diastoles and on this may be 
seen the “ff” waves. This interesting detail consists in 
small oscillations, usually regular. The “ff” waves appar¬ 
ently are found in no other condition. 

Heart-block. —In incomplete heart-block the a-c in¬ 
terval is prolonged beyond 0.3 second. In the venous 
tracing this may cause the “a” wave to coincide with the 

9 Lewis, T.: The Mechanism and Graphic Registration of the Heart Beat, 
p. 267. 



62 


MODERN CONCEPTION OF HEART DISEASE 


ventricular waves (that follow the previous auricular im¬ 
pulse) and, by their suj)erimposition, to produce an exag¬ 
gerated excursion. Variations in the a-c interval are 
common. Sometimes the impulse may be blocked and then 
there is a gap in the arterial curve and the “a” wave in 
the phlebogram is not followed by the ventricular waves. 
There may be but half or a third or fourth as many up¬ 
strokes in the arterial curve as there are “a” waves in the 
venous tracing in which the ventricle is not beating in 
response to every auricular contraction, i.e., when a 2-1, 
3-1, 4-1, or higher rhythm exists. A change from a 1-1 
to a 2-1 or higher rhythm will cause an irregularity in 
the arteriogram. If the arterial tracing is irregular in 
incomplete heart-block, examination of a sufficient length 
of the curve will show the presence of dominant rhythm. 
The irregular arteriogram of incomplete heart-block can be 
distinguished from that of flutter only by the assistance of a 
successful phlebogram or, better, by an electrocardiogram. 

In complete heart-block complete dissociation exists. 
The ventricle contracts in response to an impulse centre in 
its own tissues, and this is represented in the arterial curve 
by a series of regular waves of a frequency of about 30 to 
40 per minute, though sometimes higher or lower. In the 
jugular tracing the ventricular waves are present at their 
expected places in relation to the arterial curve, and be¬ 
tween them occur other waves. These latter, if spaced 
regularly in relation to each other, may be identified as 
“a” waves. If, on determination of the rate of the “a” 
waves and that of the arterial beats, the latter are not in 
relation to the former in a ratio of 1 to 1, 2 to 1, or higher, 
the diagnosis of complete heart-block is confirmed. An 


»■' » 111 »' " » »-» .r-Y «—•—•—v—»-■-»—»—»—»—y—«■■■ « . m 



Fig. 12. —Partial heart-block. The a-c interval is prolonged and the third, seventh, and thirteenth 
a waves are blocked; the other a waves are exaggerated due to their superimposition on waves of the pre¬ 
ceding ventricular systole. (After Sir Thomas Lewis.) 



Fig. 13. —Complete heart-block. Auricular rate 61; ventricular 31; the two rhythms are regular 
but independent of each other. Where the a wave coincides with ventricular systole a conspicuous 
summit appears. 













METHODS OF EXAMINATION 


63 


occasional dropped beat disturbs, of course, this numerical 
ratio, but the evidence that the “a” waves are in relation to 
the succeeding ventricular excursions in the venous tracing 
should make it apparent that the block, in such a case, is 
partial and not complete. 

Polygraph tracings are also taken from the apex of the 
heart, the carotid artery, and over the liver, but their im¬ 
portance does not warrant description in this limited pres¬ 
entation of polygraphy. 


CHAPTER IV 

METHODS OF EXAMINATION (concl.) 

Graphic Methods (concl.) 

ELECTROCARDIOGRAPHIC EXAMINATION 

A complete exposition of electrocardiography is be¬ 
yond the scope of this book. The literature is extensive 
and the work highly technical; he who would fit himself to 
engage in electrocardiography should acquire a familiarity 
with its literature and spend considerable time in an electro¬ 
cardiographic laboratory. 

In the words of a master, Thomas Lewis; “These 
records have placed the entire question of irregular or 
disordered mechanism of the human heart upon a rational 
basis, so giving to the worker the confidence of knowledge; 
they have influenced prognosis and have rendered it more 
exact; they have potentially abolished the promiscuous 
administration of cardiac poisons, and have clearly shown 
the lines which therapy should follow. The new clinical 
observations have stimulated and directed a host of labora¬ 
tory researches, anatomical, physiological, pathological, 
and pharmacological, of a valuable nature.” 1 

Electrocardiography is of value in clinical medicine and 
the reader should be familiar with its essential facts. The 
electrocardiogram enables one to analyze 96 to 98 per cent, 
of the arrhythmias, which is perhaps 6 to 8 per cent, more 
than can be worked out by the tracings taken by the poly¬ 
graph. It gives detailed information as to the origin and 

1 The Mechanism and Graphic Registration of the Heart Beat, by T. 
Lewis. Paul B. Hoeber, New York, 1920. 


61 



METHODS OF EXAMINATION 


65 


passage of the contraction wave over the heart. It helps 
to elucidate many points observed clinically and on which 
the pathologist cannot offer any assistance. The various 
arrhythmias frequently do not display the typical picture 
and are then not easily diagnosed by the non-instrumental 
methods of examination, and when two or more of these 
functional conditions are present in combination, the prob¬ 
lem is often too obscure for ordinary bedside diagnosis. 
The detection of impaired conduction in the ventricle and 
the accurate differentiation of the ventricular type of 
paroxysmal tachycardia from that of auricular origin, both 
of which are of distinct importance in prognosis, are de¬ 
pendent upon the use of the electrocardiograph. As 
regards which valve, if any, is affected, the electrocardio¬ 
gram offers evidence of but indirect value and not infre¬ 
quently is of no assistance. Electrocardiography may be 
said to have two distinct limitations: (1) it usually fails 

to demonstrate pulsus alternans, and (2) there are a few 
electrocardiograms which are difficult to interpret. With 
experience the latter tend to become rarer. The use of 
the electrocardiograph forms, of course, but one of the 
methods of cardiac examination, and to be most helpful, 
must be employed with the latter; it should not be allowed 
to lessen one’s efforts to make accurate diagnoses with¬ 
out this aid, but its unmasking of our failures should 
react like the post-mortem examination, to guide and stim¬ 
ulate effort towards greater efficiency in diagnosis. 

History. —It is known that when a muscle contracts, 
the contraction is accompanied by an electrical change. 
In 1855, Kolliker and Muller 2 first demonstrated, in the 

2 Kolliker, A., and Muller, H.: Verhandl. d. phys. med. GeselUch. i. 
Wurzburg, vi: 528, 1855. 


5 



66 


MODERN CONCEPTION OF HEART DISEASE 


heart of a frog, that an electrical current was associated 
with each of the contractions. The capillary electrometer 
was used to measure the current. In this instrument there 
is a column of mercury which moves up and down in a 
glass tube and may be photographed. The instrument is 
subject to the error of overshooting. In 1887, Waller 3 
made the first use of the capillary electrometer on human 
beings. The first good records with the capillary electrom¬ 
eter were obtained by Bayliss and Starling, 4 in 1892. 

The string galvanometer was introduced by Einthoven, 5 6 
of Leyden, in 1903, to replace the capillary type. This 
new instrument is so superior that it has superseded other 
forms of sensitive galvanometer. The electrocardiograph 
remained, however, largely a laboratory instrument, of 
use to the physiologist but not to the clinician. About 
1908 or 1909, Thomas Lewis, of Cardiff, Wales, became 
acquainted with the electrocardiograph in the laboratory 
of Edelmann, of Munich, and on his return to England, 
the Cambridge Scientific Instrument Company made him 
one to use. Lewis was fortunate in having the oppor¬ 
tunity to examine patients in the unusual clinic which 
James Mackenzie had built up by his fame from his studies 
of the venous pulse, and in a short time the essentials of 
clinical electrocardiography were worked out. To-day the 
electrocardiograph is widely used in clinical medicine. 

The American electrocardiograph, the Hindie, was 
started in 1917. This is now manufactured at Ossining, 
N.Y. The firm has associated with it Dr. Williams, a 

3 Waller, A. D.: Jour. Physiol., viii:229, 1887. 

4 Bayliss. W. M., and Starling, E. H.: Monthly Internal. Jour. Anat. and 

Physiol., ix: 256, 1892. 

6 Einthoven, W.t Annalen der Physik., Folge iv, xii: 1059, 1903. 



METHODS OF EXAMINATION 


67 


physicist, who has contributed very largely to the high 
quality of the Hindle machine. 

The best authorities on the physical side of electro¬ 
cardiography are Einthoven, Lewis, and Williams. 

The Instrument. —This can be understood satisfac¬ 
torily only by personal inspection. Its essential feature 
is a very fine fibre or string of quartz or glass made opaque 
by a coating of silver or platinum. This fibre is 0.002 to 
0.005 mm. in thickness. It is suspended between two poles 
of a magnet and oscillates in accordance with the passage 
of the intermittent electrical current produced by the beat¬ 
ing of the heart of the patient with whom it is in circuit. 
The string is illuminated by a powerful electric light, mag¬ 
nified (900 times in the Hindle instrument) by lenses of a 
microscope, and its oscillating shadow focussed on the front 
of a motion camera where it is photographed. 

Electrodes. —As mentioned above, the electrical 
changes in the heart were first detected by placing the con¬ 
tacts or electrodes on the exposed organ; later it was 
found that records could be obtained from the external 
surface of the chest wall; and now it has been established 
that comparable results may be secured from electrodes 
placed on the limbs. The latter is the procedure in ordi¬ 
nary clinical work. The patient is connected with the string 
by means of three electrodes,—on the right forearm, left 
forearm, and left lower leg, respectively. A common type 
of electrode is a sheet of zinc covered with a pad wet with 
warm, twenty per cent., salt solution. Another form of 
electrode consists of a porous pot filled with warm salt 
solution and well-washed cotton wool; this is surrounded 
by a larger vessel containing a saturated solution of zinc 
sulphate in which a sheet of zinc is immersed, and to the 


68 


MODERN CONCEPTION OF HEART DISEASE 


latter is soldered the leading-off wire. The patient’s hands 
and left foot are placed in the salt solution of the inner 
vessel of the respective electrode. 

Standardization of the Electrocardiogram. —The 
purpose of this is that the records taken in different labora¬ 
tories and on the same patient at different times may be 
kept to the same scale of excursion so that comparisons 
may be permissible. Einthoven’s standard, in which one 
centimetre of excursion in the final photograph is equiva¬ 
lent to one millivolt potential difference at the end of the 
recording fibre, is now universally adopted. (The neces¬ 
sary qualifications of the electrodes, the technic of taking 
the electrocardiogram, and other details are fully discussed 
by Lewis in his book, 6 to which those desiring fuller infor¬ 
mation are respectfully referred.) 

The Leads or derivations. There are three of these, 
made by a turn of a key on the switchboard of the electro¬ 
cardiograph to connect any two of the electrodes on the 
patient. Lead I is between the two arms, lead II from 
the right arm to the left leg, and lead III between the 
two left limbs. The picture obtained varies in the three 
leads; identical waves are of different amplitude. This may 
perhaps be better appreciated by examination of Figure 
14, the so-called Einthoven triangle. The three leads are 
indicated by the Roman numerals and respective limbs by 
the abbreviations R.A., L.A., and L.L. If the line A.B. 
represents the action current in the heart at a given mo¬ 
ment, it will be represented in the respective leads as 
excursions of the size indicated by the lines A'B' placed 
on the sides of the triangle. In accurately taken electro- 

9 The Mechanism and Graphic Registration of the Heart Beat, Paul B. 
Hoeber, New York, 1920. 



METHODS OF EXAMINATION 


69 


cardiograms, it has been shown that the height of any 
individual wave in a single lead can be calculated from its 
values in the other two leads; for example, the height of 
a wave in lead II is equal to the sum of its excursions in 
lead I and III, etc. 

Leads I and III are of value chiefly for the QRS com¬ 
plex and the determination of ventricular preponderance. 



Fig. 14.—The Einthoven triangle, indicating diagrammatically the relation of 
the three leads to the heart. 


Practically all other conclusions may be drawn from lead 
II, which is therefore the most important derivation. It 
will be noted that lead II is much more nearly parallel to 
the anatomical axis of the heart; the electrical and anatom¬ 
ical axes do not, however, coincide exactly. 

The Normal Electrocardiogram. —The electro¬ 
cardiogram is a photograph of the oscillations of the string 







70 


MODERN CONCEPTION OF HEART DISEASE 


of the galvanometer caused by changes in the electrical 
potential as the excitation wave passes over the heart. At 
first sight (Fig. 15), it looks like a zigzag line, but on closer 
study, it can be seen that the departures from the base 
line are repeated in a regular order. These departures 
from the base line have been named in an arbitrary manner 
(before their significance was known) the P, Q, R, S, T and 
U waves. 

The waves are termed upright or inverted according as 
they are above or below the base line. When there is no 
current passing through the string, the image of the latter 
is flat, and the position is designated as isoelectric. 

The background of the electrocardiogram is ruled into 
squares. The horizontal lines are known as the Ordinates 
and are produced by lines engraved on the lens in the 
camera. They make it possible to measure the excursion 
of the waves from the base line and thus, in electrocardio¬ 
grams taken in the standardized manner, to determine the 
electromotive force. The distance of each ordinate indi¬ 
cates an electromotive force of one tenth of a millivolt 
(0.0001 volt) which is often written l 10 ' 4 volt. Every fifth 
ordinate is heavier as an aid to the eye. The vertical rul¬ 
ings are the Abscissa, which permit measurement of the 
waves in respect to their duration in time. The fine-fined 
abscissas mark off periods of one twenty-fifth of a second, 
while the heavier ones, i.e., every fifth, indicate one fifth 
(0.2) second. These abscissas are made by the time 
marker, a revolving wheel, whose spokes, at the above inter¬ 
vals, cut across the stream of light in the electrocardiograph. 
The rate of the heart beat per minute is determined by 
counting the number of times some definite wave, usually 
the R wave, is repeated. A convenient method is to count 










































































































































































































Fig. 16.—Ventricular preponderance. 

Left electrocardiograms—leads I and III from a case of cardiovascular syphilis with aortic 
regurgitation. The index is +32.5, indicating left preponderance. The inverted T wave in lead I 
is a digitalis effect. 

Right electrocardiograms-—leads 1 and III from a case of rheumatic heart disease with mitral 
stenosis. The index is —27, indicating right preponderance. 
























































































































































































































METHODS OF EXAMINATION 


71 


the number of H waves occurring in six seconds (thirty 
successive fifths of a second in the tracing) and then to 
multiply this number by ten, for the rate per minute. 

The P Wave is associated with the contraction of the 
auricles. It must be upright in lead II, and not more than 
three tenths of a millivolt in force or more than one tenth 
of a second in duration. The occurrence of a notch in the 
P wave does not indicate abnormality. The P wave is 
usually upright in lead I but is often very small and may be 
flat or isoelectric; in lead III it may be diphasic (showing 
an excursion on both sides of the base line) or split. In¬ 
version of the P wave in lead II indicates that the impulse 
did not start from the sino-auricular node; the more defi¬ 
nitely inverted is the P wave, the nearer to the node of 
Tawara is the new impulse centre assumed to be. 

The P-R Interval indicates the period of conduction 
between the auricle and the ventricle. It is found by 
measuring from the initial deflection of the P wave to the 
initial deflection of the succeeding II wave. Normally, 
the interval varies from 0.12 to 0.18 second, though Lewis 
has recently extended its maximum length to 0.21 second. 
It is a safe rule that if the P-R interval exceeds 0.2 second, 
which is just equal to the space between the coarser lines 
made by the time marker, one is dealing with some degree 
of A-V heart-block. 

The QRS Complex is the result of the initial spread 
of the excitation wave in the ventricle. The Q and S 
Waves may be small or absent and are relatively unim¬ 
portant in ordinary clinical work. 

The R Wave is a sharp upward spike and is usually 
the most prominent wave in the electrocardiogram. It is 
abnormal if it has a duration of more than 0.1 second, or 


72 


MODERN CONCEPTION OF HEART DISEASE 


if it is much thickened and notched in lead II. Simple 
notching is not infrequent in leads II and III in normal 
electrocardiograms. 

The T Wave is the end deflection of the ventricular 
complex. It is produced by the decline of the state of 
excitation in the ventricular muscle; but further than this 
its exact meaning is as yet somewhat obscure. Normally 
the T wave should be upright in lead II. 

Flattening or inversion of the T deflection has been 
found associated with weakness of the myocardium and 
with hypothyroidism, and particularly as a sign of the 
action of the drug digitalis. The depression of the T wave 
due to digitalis (present in figure 23 lower curve, 24 upper 
curve, and 25) is of a progressive nature, the wave being 
first flattened and then inverted. The depression includes 
both the T wave and some of the string shadow just preced¬ 
ing. T of the normal ventricular complex is a combina¬ 
tion of right and left ventricular effects; the former tends 
to make T negative; the latter, positive . 7 

The U Wave is a small inconstant deflection which 
occurs just after the T wave, in slow-acting hearts. It is 
not well understood and appears to be unimportant. 

The beginning of the first heart sound commonly coin¬ 
cides with the descending limb of the R wave, while the 
second sound commences at about the end of the T deflec¬ 
tion. It has been demonstrated in experimental work 8 on 
dogs that the upstrokes of the P and II waves precede the 
evidence of muscular contraction in the auricle and ventri¬ 
cle, respectively, by about 0.02 to 0.04 second. 

7 Wilson, F. N., and Hermann, G. R.: Heart, viii, 3:274 (May, 1921). 

8 The Mechanism and Graphic Registration of the Heart Beat, by T. 
Lewis. Paul B. Hoeber, New York, 1920, p. 51. 



METHODS OF EXAMINATION 


73 


Ventricular Preponderance. —This term is used to 
indicate relative increase in the weight of one ventricle as 
compared with that of the other. It is not synonymous 
with hypertrophy, as in the latter condition the whole heart 
may be hypertrophied, but if the balance is not disturbed 
there is no preponderance of right or left ventricle. In 
the careful study by Lewis and Cotton of cardiac hyper¬ 
trophy (which will be considered in Chapter XVIII), it 
has been demonstrated that the presence in the electro¬ 
cardiogram of the feature termed ventricular preponder¬ 
ance is very reliable evidence of an increase in weight of 
the ventricular muscle. Certain American investigators, 0 
however, have found that a relation between the form of 
the electrocardiogram and the relative weights of the ven¬ 
tricles does not exist unless the whole heart weighs over 
250 gm. and then the relation is not a close one. 

Ventricular preponderance is diagnosed (Fig. 16) 
from the study of the QRS complex in the first and third 
leads. If R is high in lead I, and has a downward deflec¬ 
tion in lead III, preponderance of the left ventricle is 
suggested; the reverse of these conditions indicates right 
preponderance. Certain authors have doubted the accu¬ 
racy of the above generally accepted interpretation. 

When preponderance is present, it is possible to obtain 
a numerical estimate of its extent, or the Index, by means 
of formula. Thus, (Ri+S 3 ) - (R 3 +Si) = index . 10 In this 
formula Ri is the height above the base line of the R wave 
in lead I, as measured by the millimeter ordinates on the 
electrocardiogram; S 3 indicates the depth of the S wave in 

0 Wilson, F. N., and Hermann, G. R.: Jour. Amer. Med. Assn., 78, 23: 1839 

(June 10, 1922). 

18 White, P. D., and Bock, A. V.: Amer. Jour. Med. Sci., v, 156: 17, 1918. 



74 


MODERN CONCEPTION OF HEART DISEASE 


lead III, etc. This is merely subtracting the right ventric¬ 
ular values from those of the left. An index of +20 to 
+30 usually indicates left preponderance, while above +30 
is always left preponderance. Values of -15 to -18 are 
usually evidence of right ventricular preponderance, and 
beyond -18 is always so. The variation in the position of 
the heart as affected by the height of the diaphragm, res¬ 
piration, etc., makes a difference in the above index and yet 
not enough to account for the higher figures. This matter 
of ventricular preponderance does not take into considera¬ 
tion the depth of the heart mass, and on theoretical grounds 
there is much that is unsound, and yet the conception 
proves useful. 

Sinus Arrhythmia. —The auricular and ventricular 
waves are present and in normal relationship to each other, 
but the former, the P waves, are irregular in their rhythm. 
It is an arrhythmia in which the irregularity involves the 
whole heart and is due to a failure of the pacemaker, i.e., 
the sino-auricular node, to start an excitation wave at 
regular intervals. The electrocardiogram shows the usual 
normal waves, but the groups representing the individual 
heart cycles do not maintain the customary regular spacing. 
The usual form of sinus arrhythmia is that in which the 
waves show a rhythmic acceleration and slowing, in accord¬ 
ance with inspiration and expiration. Sometimes a simul¬ 
taneous waxing and waning of the height of the II waves 
is seen, due to the respiratory shifting of the position (and 
so of the relation of the cardiac electrical axis to the lead 
in use) of the heart. A less frequent type, termed phasic, 
is similar save that the acceleration and slowing do not con¬ 
form to the respiratory curve; they commonly extend over 
somewhat longer periods. 



Fig. 17.—Sinus arrhythmia 























































































a 

a 

cT 

> 

ci 

£ 

”3 

5 

Urn 

o 


>s 


o 

>i 

tm 

o 

> 

W 


d 

a> 

-a 

0) 

fa 

3 

d 

s 


d 

3 

- 

*E 

3 

t 


a 


METHODS OF EXAMINATION 


75 


Sino-auricular Block. —In this condition some of 
the P waves appear to be absent or delayed. A common 
type of electrocardiogram is that in which the frequency of 
the waves is suddenly cut approximately in half. The P, 
R, and T waves are all present, but the above change in 
their frequency is the striking feature. In other instances 
a single or several beats appear wanting. This resembles 
the dropping of beats that takes place in certain cases 
of auriculo-ventricular heart-block, but is distinguishable 
from the latter by the fact that in sino-auricular block the 
P wave is missing as well as those of the succeeding ven¬ 
tricular complex. In many instances of sino-auricular 
block, the phenomenon of ventricular escape 11 occurs; in 
other words, if the stimulus to contract does not come from 
the sinus node in due time, the ventricle may beat in re- 
sponse to an impulse from a lower centre, usually the 
auriculo-ventricular node. The change of the place of 
origin from the sinus to the A-V node is often expressed 
as a shifting of the pacemaker. The electrocardiograms 
of instances of sino-auricular block may at times be quite 
complex and require care in their interpretation. 

Atrio-ventricular Rhythm or Nodal Rhythm.— 
When this is present the auricle and ventricle are contract¬ 
ing more or less simultaneously in response to impulses 
originating in the A-V node. The condition has been 
referred to in the discussion of sino-auricular block. The 
P wave is usually inverted, often distinctly so, but it is not 
always readily seen, as it may be buried in the ventricular 
complex. The contraction of the auricle may slightly pre¬ 
cede, coincide with, or follow that of the ventricle; conse- 

11 Some authors have restricted the term to the response of the ventricle 
to an impulse originating on the ventricular side of the A-V node. 



76 


MODERN CONCEPTION OF HEART DISEASE 


quently the P wave appears in these relationships to the 
ventricular complex of the electrocardiogram. Atrio¬ 
ventricular rhythm is not common; it is hardly to be diag¬ 
nosed save by the graphic methods. 

Premature Beats, or Extrasystoles. —These are 
heart beats which occur prematurely and do not form part 
of the rhythmic series of beats. They may arise from a 
focus in the auricle or in the ventricle, and occasionally in 
the A-V node. Their recognition is usually easy in the 
electrocardiogram. With the ventricular extrasystole, the 
ventricular complex is aberrant or abnormal in form, but 
in the case of the auricular and rarer nodal extrasystole, 
the succeeding ventricular complex is represented by nor¬ 
mal waves. In exceptional instances, aberration of the 
ventricular waves may occur even though the extrasystole 
be of auricular origin; this is explained as probably due to 
impairment of conduction in the ventricular muscle, which 
has not fully recovered from the previous contraction. 
With the auricular extrasystole there is also evidence of the 
presence of a P wave, though the latter usually is differ¬ 
ent from the normal wave starting from the sino-auricular 
node. According to the degree of prematurity of the 
auricular extrasystole the P wave of the ectopic beat is 
advanced nearer to the preceding T wave, or it may be 
superimposed upon the latter. The variation in the length 
of the pause after the premature beats has been discussed 
in the j)receding chapter; the length of the pause is of 
less importance in the electrocardiogram. 

Paroxysmal Tachycardia. —This arrhythmia may be 
defined as a regular tachycardia with an abrupt onset and 
cessation. Arbitrarily it is limited to regular tachycardias 


Fig. 19. —Ventricular premature beats, interrupting normal rhythm. The ectopic beats are aberrant in form and are indicated by an * placed below. 





















































































































































































































Fig. 20. —Paroxysmal tachycardia. Above, auricular type; centre, from ventricle; and below, 
of indeterminate origin. 
























































































































































































































































METHODS OF EXAMINATION 


77 


not exceeding 200 per minute, though occasional cases of 
slightly more rapid rate are best assigned to this arrhythmia. 

The paroxysm most commonly arises in the auricle, but 
may have its origin in the A-V node, or in the ventricle. 
Paroxysms of supraventricular origin nearly always have 
ventricular complexes of normal appearance; rarely, aber¬ 
ration may occur when the impulses rise in the auricle 
but follow an abnormal course in the ventricle. In the 
auricular type, the P wave is always abnormal, which is 
further evidence of its ectopic origin; usually it is inverted. 
In many cases the P wave is buried in the ventricular com¬ 
plex. If the electrocardiogram shows only the paroxysm, 
it is not always possible to determine the point of origin 
of the tachycardia; when the onset of the new rhythm is 
shown, the type of premature beat, of which the paroxysm 
apparently is a series, may be represented and its origin 
determined. 

If the ventricular complex is aberrant (abnormal) in 
form, the paroxysm is probably of ventricular origin. 
Further evidence may be obtained from a study of the P 
waves, if present. An electrocardiogram showing the 
onset of the paroxysm may not be available, but if a record, 
taken when the attack is not present, discloses ventricular 
extrasystoles of which the ventricular complexes of the 
paroxysm are an exact replica (such was the case in the 
middle curve of Fig. 20), the ventricular origin of the new 
rhythm is almost certain. The ventricular type of parox¬ 
ysmal tachycardia, unlike the commoner auricular form, is 
of distinctly bad prognostic import because of its frequent 
association with occlusion of the coronary artery and infarct 
of the myocardium. Robinson and Hermann 12 have em- 


n Robinson, G. C., and Hermann, G. R.: Heart, viii, 59:1921. 




78 


MODERN CONCEPTION OF HEART DISEASE 


phasized the need of an electrocardiogram to make this 
important differentiation. 

Auricular Flutter. —In this condition the auricle 
beats at a rapid and regular rate, which varies in human 
subjects from 200 to 365 per minute. The average rate 
is about 300. The electrocardiogram is important in the 
diagnosis of auricular flutter, as the latter can rarely be 
recognized save by the use of instrumental methods of 
examination, and the polygram is often unsatisfactory due 
to insufficient excursion of the waves. The auricular waves 
are represented by a continuous series of P excursions, giv¬ 
ing to the picture of the string a regular zigzag appearance 
interrupted by the ventricular complexes. When the ven¬ 
tricle is beating at a rapid rate and in less favorable leads 
(lead I, and sometimes lead III) the superimposition of 
the ventricular waves on the series of P waves may obscure 
the regularity of the latter. The electrocardiogram shows 
constant activity of the auricle, but that of the ventricle is 
less frequent. Thus, 2 to 1, 3 to 1, or higher ratio main¬ 
tains; in a certain sense auriculo-ventricular heart-block 
is present, but that the latter is not the primary or essential 
rhythm is readily evident from the abnormally high rate 
of the auricular waves. It is emphasized that the auricular 
waves show a high degree of regularity; those of the ventri¬ 
cle may be regular or irregular, the latter resulting from 
a variation in the rate of response to the supraventricular 
stimuli. The ventricle rarely responds to all of the auricu¬ 
lar contractions and, if so, only for a short time; so high a 
ventricular rate is incompatible with the power of the ven¬ 
tricular muscle and the maintenance of the circulation. 

Auricular Fibrillation. —In this frequent and im¬ 
portant arrhythmia there is always some part of the auric- 


p IQ 21 —Auricular flutter. In the upper electrocardiogram the ventricular response shifts from 5 to 1 to 3 to 1, thus causing an irregularity. 
In the lower tracing the ventricular rate is regular and just half that of the fluttering auricle. 


























































































































































































































Pj G> 22 .—Auricular fibrillation. In the lower curve many of the coarse oscillations are shown. 






















































































































































METHODS OF EXAMINATION 


79 


ular musculature that is in process of contraction, but co¬ 
ordinate systole of the auricle is in abeyance. It is now 
known that the mechanism of auricular fibrillation (See 
Chapter XVII) is essentially the same as that of auricular 
flutter, but in the former the more rapidly travelling waves 
follow sinuous paths. The rate of the auricular waves in 
fibrillation averages 450 per minute. 

Auricular fibrillation is readily recognized in the elec¬ 
trocardiogram by the irregular spacing of the R waves and 
the absence of the normal P waves. The shadow of the 
string between the successive R-T complexes, namely, dur¬ 
ing ventricular diastole, varies in the photograph from a 
flat line to oscillations which may for a few cycles simulate 
closely the zigzag line seen in flutter. Where the auricu¬ 
lar waves are coarse and comparatively regular the condi¬ 
tion is termed the flutter-fibrillation type of fibrillation, 
and by some, impure flutter. It is characteristic of fibrilla¬ 
tion that coarse, regular waves, 13 if present, are not so in 
all of the heart cycles; it is still customary to limit the 
term auricular flutter to those electrocardiograms show¬ 
ing an absolute and continuous regularity of the auric¬ 
ular complexes. 

In typical uncomplicated cases of auricular fibrillation, 
the ventricular rate is usually well over one hundred and 
the irregularity is evident, but when some degree of A-V 
heart-block is present, as when digitalis therapy is in opera¬ 
tion, the ventricular rate is lower and may be remarkably 
regular. Then the absence of normal P waves and the 
irregular appearance of oscillations during the interven- 

13 They are present in leads taken directly from the chest wall; such leads 
are more favorable than limb leads for the study of articular activity. 
Heart, viii, 1921. 



80 


MODERN CONCEPTION OF HEART DISEASE 


tricular periods of the curve is of distinct assistance in 
differentiating fibrillation from atrio-ventricular rhythm 
with P waves buried in the ventricular complexes. 

Ventricular Fibrillation. —This arrhythmia is in¬ 
compatible with the continuance of the circulation and 
nearly always results in the prompt death of the patient. 
As a result it is rarely seen except in records taken just 
before death. The shadow of the string shows excursions 
that are abnormal in outline and irregular in spacing. In 
ordinary clinical work this arrhythmia is unimportant, in 
the sense that it is not met in the surviving patient. 

Heart-block;. —This term is applied to defective con¬ 
duction between the auricles and ventricles. Heart-block 
may be partial or complete. Partial heart-block is de¬ 
tected in the electrocardiogram by prolongation of the P-R 
interval, i.e., the latter exceeds 0.21 second. If the P-R 
interval is as much as one second it is more likely that the 
ventricle has escaped, or, in other words, did not beat in 
response to that auricular contraction, but to an impulse 
originating in the A-V node. In complete heart-block the 
contractions of the auricles and ventricles are independent 
of each other. This should be suspected in the electro¬ 
cardiogram if the P waves appear to have no definite rela¬ 
tion to the ventricular complexes, and is confirmed if, on 
ascertaining their respective rates, the auricular and ven¬ 
tricular waves bear no arithmetical ratio to each other. 
Thus, if the heart-block is not complete the frequency of 
the P waves should be to the QRS waves as 1 to 1, 2 to 1, 
3 to 1, 4 to 1, etc. An exception to this occurs in partial 
heart-block when the ventricle fails to reply to certain of 
the auricular contractions, which are then said to be blocked 
and result in dropped beats (of the ventricle). A tracing 


Above, the P-R interval is prolonged to 0.24 second. 










































































































































































































Fiq. 24.—Above. Complete aurieulo-ventrieular heart-block. Auricular rate 79. ventricular 43. 

Below, Intraventricular block, right bundle branch, In this lead, lead I, the P wave happened to be isoelectric. 


























METHODS OF EXAMINATION 


81 


of this condition shows that the ventricle beats in response 
to many or most of the auricular contractions, and the 
condition of absolute independence, i.e., complete heart- 
block, is not, therefore, present. The dropped beats of 
heart-block differ from sino-auricular block in that the 
P waves are present and it is only the ventricular complex 
that is absent. Variation in the P-R interval is common; 
after the longer pauses there is often a shortening of the 
P-R interval and then the latter may show a gradual or 
rapid lengthening, as the case may be, until the P wave 
is not followed by a ventricular complex, i.e., the P wave 
is blocked and the ventricular beat dropped. 

It has been shown 14 that in heart-block the susceptible 
region is the junction of the A-V node (node of Tawara) 
with the auricular tissues or in the node itself. In complete 
heart-block the ventricle beats in response to impulses 
originating in its own tissues. The rate of this new rhythm, 
known as idio-ventricular rhythm, is slow, averaging about 
thirty per minute. In such cases the level of the block is 
supposed to be below the A-V node and the new impulse 
centre below this in the auriculo-ventricular bundle. In 
some instances, however, complete dissociation is present 
with a higher ventricular rate, forty to fifty or even ninety 15 
per minute. It seems probable that the block is then at a 
higher level and the impulse centre in the auriculo-ventricu¬ 
lar node, which possesses a higher rate of impulse formation 
than does the conduction bundle on the ventricular side of 
the node. In either case the ventricular complex appears 
normal in the electrocardiogram since the ventricle is still 

14 Lewis, T., Meakins, J. C., and White, P. D.: Heart, v:289, 1913-14. 

15 The Mechanism and Graphic Registration of the Heart Beat, by T. 
Lewis. 1920. Paul B. Hoeber, New York, p. 306. 

6 



82 


MODERN CONCEPTION OF HEART DISEASE 


responding to supraventricular stimuli, i.e., above the divi¬ 
sion of the auriculo-ventricular bundle into the right and 
left branches. 

Intraventricular Block, or impaired conduction in 
the branches of the bundle of His, is indicated if the QRS 
complex exceeds 0.1 second. Notching and thickening 
of the wave is also usually present. The T wave, or end 
deflection, in bundle branch block is opposite in direction 
from that of the initial wave of the ventricular complex. 
If the direction of the QRS complex resembles that found 
in left ventricular preponderance (which see), it is com¬ 
monly held that the lesion is located in the right bundle 
branch, and in the left bundle if the waves simulate those 
of right preponderance. 

A block of the right branch is found much more fre¬ 
quently than is one of the left branch. (In fact the latter 
is very rare.) The usual reason given for this is that the 
left branch spreads out promptly into a broad sheet and 
consequently would require a lesion of greater extent than 
would be necessary to block the branch on the right side, 
which remains for a space as a comparatively compact 
bundle. The anatomical studies of Gross, 16 however, sug¬ 
gest another explanation. He finds that the right branch 
of the A-V bundle invariably receives its blood supply from 
the left coronary artery by a stout vessel called the ramus 
limbi deoctri, which is a terminal artery, while the left 
branch of the bundle has no specific blood supply of its 
own, but is nourished by profuse anastomoses of vessels 
from both sides. 

The mistake must not be made of diagnosing prepon- 

16 Gross, L.: The Blood Supply of the Heart, in Its Anatomical and 
Clinical Aspects, New York, Paul B. Hoeber, 1921. 




rr 

OQ << 
ri* ^ 

E. cr 

• cr r re cr 
re 5-0 
(T >_> 53 “5 

K- 5* - 

3 re T3 p 
<2 ?*§. 

&»£§. 

(Ts'rS 


- . . 5? 
3 <S 7- cr 
2 S-cri 
R » — CP 

p p o £. 

?T" 


- TB 

tr I —— 

cr<n c . 
o -» •o < 

<-*■ J- 2 

cr cl o d 


rc "• o" o 
o <-*.«< c 

3 re » 5 

p O % g 

5.7 

3 5 3.£ 

W o v 

p? £-1 

§ C E o 

ce V' 
rD 


C- » 3 

ft P"< 

•O O _ 

-I jj P 



a 5 ’ 

ft 

09 << 

H 

C"C- 

35 

o ft 

p 

7T _* 

< 

P ° 

ft 

d a- 



p* 

_►» pv 


o ^ 

cr 


o 

cr “ 

cr 

o 

<_». 


p 

*© 

2 . 

5 * 

o 

OQ 

CD 

- 

V. 

§ 


Cl 

CL 


P 

•“ 1 

(t 

r-r 


o 































































































































































METHODS OF EXAMINATION 


83 


derance of either ventricle, as a lesion causing a block in 
one bundle branch will, by forcing the impulse to travel 
by the opposite bundle, give the picture of a levo- or dextro- 
cardiogram, although hypertrophy of neither side of the 
heart may exist. Ventricular preponderance and intra¬ 
ventricular block cannot both be diagnosed in the same 
electrocardiogram. 

Arborization Block has been described, but it is 
doubtful if it occurs. The term is used to indicate a lesion 
in the Purkinje network of the ventricles, and to account 
for certain aberrant forms of the ventricular complex. It 
has been shown 17 that an incomplete block in one of the 
main branches of the auriculo-ventricular bundle gives rise 
to ventricular complexes that are transitional in form be¬ 
tween the normal complex and that of a complete bundle 
branch block. The same observers state, “A lesion of the 
Purkinje plexus or of the smaller subdivisions of the His- 
bundle might be expected to have about the same effect 
upon the activation of the ventricular muscle that the liga¬ 
tion of a freely anastomosing artery has upon the blood 
flow in the region that the artery normally supplies.” 

Combined Arrhythmias. —It frequently happens that 
more than one arrhythmia may be present in an individual 
heart. As might be expected, this may cause a most ob¬ 
scure clinical picture; in the electrocardiogram, however, 
the analysis is usually clear. The same methods of inter¬ 
pretation described for the arrhythmias, when occurring 
singly, are to be used. Two examples are pictured in 
Fig. 25. 


17 Wilson, F. N., and Hermann, G. R.: Heart, viii, 3:229 (May, 1921). 



CHAPTER V 
THE NORMAL HEART 

The term “normal heart” does not apply to a closely 
circumscribed standard to which every heart must conform 
or be classed as abnormal. On the contrary, the heart 
normally varies, as do other organs, between individuals, 
and especially in accordance with age, sex, stature, muscu¬ 
lar development and manner of living of the individual in 
whom it is located. If called upon to decide upon the 
normality of a patient’s heart, the physician can give his 
opinion with safety only after taking a reasonable history 
and making a careful examination. 

History. —The anamnesis may or may not contain the 
presence of a disease of etiological significance as regards 
the heart, and yet of course that organ may have escaped 
unscathed. Judgment is required in interpreting whether 
some symptoms which may be described by the patient are 
due merely to the overtaxing of a normal heart or are the 
early symptoms of cardiac failure. If, however, there is 
a history of the progressive increase of the above symptoms 
during smaller and smaller amounts of physical exertion, 
grave doubt should exist as to the normality of the heart. 

Apex Impulse. —In most normal hearts, the apex 
imjmlse is palpable and frequently visible in the fifth inter¬ 
space a little within the left midclavicular line, if the patient 
is sitting or standing, and one interspace higher, if the 
patient is lying. The true apex of the heart lies slightly 
(1 cm. perhaps) lower and internal to the outer limit of 
the palpable impulse. The apex impulse or cardiac im- 

84 


THE NORMAL HEART 


85 


pulse frequently extends over both the fourth and fifth 
interspaces inside the midclavicular line, and in such a case 
the point of maximum impulse, it should be remembered, 
is above and internal to the true apex. There is consider¬ 
able variation, in healthy individuals, in the force of the 
apex impulse, since the transmission is much influenced 
by the thickness of the parietes, the width of the intercostal 
spaces, and the convexity of the chest. Pulmonary em¬ 
physema may mask the impulse of a normal heart. The 
heart may be normal hut the apex impulse displaced, if 
ptosis of the organ is present or if the heart is pushed or 
pulled from its normal location by outside influences, such 
as pleural effusion, pneumothorax, pleural adhesions, ab¬ 
dominal tumor, etc. 

The apex impulse is usually palpable as a single shock, 
but it is not uncommon to note the presence of a slight 
to moderate vibration systolic in time. This vibration, 
which is sometimes termed a thrill, is most common in 
young adults, especially when the heart is beating vigor¬ 
ously after exercise or excitement. It should be sharply 
distinguished from the definite purring thrill which accom¬ 
panies many cases of mitral disease. 

Normally the apex impulse is mobile, with change of 
position of the patient. If the latter is examined while 
lying on one side and then on the opposite, the mobility of 
the apex varies from a half to one and a half inches. 

Borders of Cardiac Dulness. —The outer limit of 
the percussion dulness of the heart varies somewhat in 
health. It is particularly dependent, of course, on the 
position of the heart, which, as demonstrated by radiog¬ 
raphy, is influenced by the height of the diaphragm, etc. 
Furthermore, a distinct difference in the location of the 


86 


MODERN CONCEPTION OF HEART DISEASE 


borders of the heart dulness has been shown to result from 
a difference in the method of percussion employed. Since 
it is known that “there is no normal heart, but the heart 
fits the patient,” it is more informing to state the relation 
of the heart border to certain landmarks of the chest. 
Thus, when using average light percussion and noting the 
outer limit of slight hut distinct dulness, the border of 
the heart will be found in the fifth interspace, about at 
the left midclavicular line (nipple line is sufficiently accu¬ 
rate in the male sex); from thence the left border extends 
upward with a slight inward convexity to the second inter¬ 
costal space at about 2 to 3 cm. from the sternal margin; 
and from this point, the percussion outline sweeps down¬ 
ward to a point in the fourth intercostal space, averaging 
2 cm. beyond the right edge of the sternum. Below this, the 
cardiac border usually curves inward to merge with the 
liver dulness. 

The percussion note of dulness will gradually change 
to that of flatness as the pleximeter finger is moved pro¬ 
gressively inward and the examination is continued to the 
part of the heart between which and the chest wall there 
is no interposition of lung tissue. This area of the pre- 
cordia is termed the superficial cardiac space , in distinction 
to the deep cardiac space which encircles it and whose 
outer border has been detailed above. The limits of the 
superficial cardiac space, easily determined by the point 
at which the percussion note changes to flatness, is depend¬ 
ent, obviously, upon the contact of the heart with the chest 
wall and is much influenced by conditions of increased pul¬ 
monary volume, such as emphysema. It is sufficiently 
accurate to state its outlines in health, as extending from 
the apex of the heart to the fourth left costal cartilage and 


THE NORMAL HEART 


87 


downward in the median line. Because of the influence 
of the sternum on the transmission of the lung resonance, 
the right border of the superficial cardiac space, as deter¬ 
mined by percussion, is a little to the left of the line where 
the right lung is in anatomical relation to the heart. 

Supra cardiac Dulness.— Percussion at the base of 
the heart over the great vessels gives varying results in 
healthy individuals. There may be but slight dulness or 
a well-marked dull area about 4 to 6 cm. wide, depending 
upon the proximity of the aorta and pulmonary artery. 
This area is commonly determined at the level of the second 
interspace, but it should be remembered that the anatomical 
position of the beginning of the great vessels is nearer to 
the third interspace. In drawing conclusions from the 
results of percussion over the base of the heart, due allow¬ 
ance must be made for the conditions known to influence 
the relations of the aorta and pulmonary artery to the wall 
of the chest. 

Since the heart and its percussion findings in health 
are subject to so much variation, it does not seem profit¬ 
able to attempt to memorize any definite set of figures or 
landmarks. It may have been noted that the writer has 
not recommended any one method of percussion as being 
superior, and it is suggested that the reader continue to 
employ the method in which he is most skilled. In so do¬ 
ing, experience will gradually demonstrate what data are 
normal for percussion, as performed by his method and by 
him. With such a conception of percussion, and espe¬ 
cially if the findings are checked at intervals by radio- 
graphic examination, percussion, in spite of its limitations, 
will remain a useful method of cardiac examination. 

Heart Sounds. —The first and second heart sounds 


88 


MODERN CONCEPTION OF HEART DISEASE 


follow in a rhythmic order which is usually sufficiently 
definite to permit of their differentiation. In comparison 
with the second sound, the first at the apex is longer, of a 
lower pitch, louder, and of a booming quality, as opposed 
to the more clicking or valvular quality of the second 
sound. At the base, the first sound is usually not longer 
than the second, and loses much of its booming quality, 
while in loudness, the second sound takes precedence. 
Phonocardiography has shown that the first sound at the 
apex precedes that at the base by 0.06 to 0.07 second. This 
is explained as due to the fact that the anatomical relations 
of the heart to the chest wall at the base are such that the 
initial vibrations of the first sound, which are small, are 
lost in conduction. 

The first heart sound may begin with a crescendo tone 
or acute accent which closely simulates the crescendo mur¬ 
mur of early systole so often present in mitral stenosis. 
In other instances the sound may appear to have two 
distinct phases and is described as “split.” On accelera¬ 
tion of the heart rate by exercise the apparent split¬ 
ting disappears. 

The aortic and pulmonic second sounds, best heard over 
the second right and second left intercostal spaces, respec¬ 
tively, vary in their relative loudness. In childhood, the 
pulmonic second sound is louder than the aortic, but after 
the age of twenty years, the latter gradually becomes the 
louder of the two. In old age, the aortic second sound in 
health is nearly always louder than the pulmonic. An 
individual second sound at the base may be accentuated 
but not necessarily louder than its fellow. The criterion 
on which to decide if accentuation is present is if the inten¬ 
sity of sound exceeds that which would be expected in the 


THE NORMAL HEART 


89 


heart under examination. The term accentuation is, there¬ 
fore, applied according to judgment based on experience. 
It should be emphasized that an accentuated second sound 
at the base does not necessarily indicate disease; the pul¬ 
monic second sound was found to be accentuated in three 
per cent, of 17,200 recruits at Camp Grant, Illinois, with 
apparently normal hearts. 1 Some reduplication of the 
second sounds may be present at the slower cardiac rates. 

Third heart sound. —A faint low-pitched sound is some¬ 
times audible just after the second sound, from which it 
is separated by a period of 0.02 to 0.08 second. 2 It is best 
heard by auscultating just outside the apex, immediately 
after the patient has assumed the left lateral recumbent 
posture. Elevation of the limbs (by an assistant) intensi¬ 
fies the sound. If the heart rate is relatively slow, the third 
sound is more likely to be audible. Thayer 3 reported its 
presence in 65 per cent, of individuals under forty years 
of age, but the writer has not succeeded in finding this 
third sound so frequently. 

A systolic murmur at the apex is a feature of many 
normal hearts. If it is not associated with signs of cardiac 
enlargement or with the history of etiologic significance 
as regards cardiac affections, the murmur may often be 
disregarded. There may also be a systolic murmur at the 
base, in hearts which are not abnormal. A particularly 
common form, in children, appears to be due to pressure 
of the surrounding structures on the infundibulum and 
pulmonary artery. 

1 Pardee, H. E. B. : Amer. Jour. Med. Sci., clviii: 319, 1919. 

2 Reid, W. D.: “The Auricular Heart Sounds,” Jour. Amer. Med. Assn., 
76, 14: 928 (April 2, 1921). 

3 Thayer, W. S.: Arch. Int. Med., 4:279, 1909. 



90 


MODERN CONCEPTION OF HEART DISEASE 


Blood Pressure. —There is no absolute level, above or 
below which the arterial blood pressure is abnormal. The 
height of the blood pressure in health varies according to 
age, sex, and many physiological conditions. Thus the 
pressure level may rise ten, twenty, or more points due to 
the temporary contraction of some of the muscles in the 
arm, or to excitement, etc. Inequality of the pressure on 
the two sides of the body, again, may have a physiological 
explanation. The systolic pressure is usually higher and 
the diastolic lower in the femoral than in the brachial artery. 
It must not be thought that the height of the systolic blood 
pressure, or even the pulse pressure, represent in any accu¬ 
rate manner the actual output of the left ventricle, as there 
are too many other factors influencing the peripheral pres¬ 
sure. In a rough way it may be said that the systolic 
pressure should not continuously exceed: 100 to 110, at the 
age of 10 to 15 years; 115 to 125, at 25 years; 135 to 145, 
at 40 years; and 145 to 155, at the age of 50 or more. The 
diastolic averages 60 to 75 at 10 to 15 years, and gradually 
tends to rise to 85 to 95; it should not exceed 100 at any age. 

The Exercise Tolerance should be sufficient to en¬ 
able the patient to carry on his daily life without untoward 
symptoms. Experience is the best guide on which to 
judge how much work a given heart should be expected 
to do without disturbance. The matter is further dis¬ 
cussed in the preceding chapter. 

On Rontgen Examination the normal heart varies 
in size in accordance with the size of the individual in whom 
it is placed. There are, therefore, no actual dimensions 
which may be said to be normal. The ratio between the 
transverse diameter of the heart and the internal diameter 
of the chest should not exceed 53 per cent. 


CHAPTER VI 

THE CLASSIFICATION OF HEART DISEASE 

Until recently the diagnosis of affections of the heart 
was limited mostly to an estimate of the structural change 
or pathology that was present. The cause of the disease 
and the functional condition of the heart are even more 
important, for upon a knowledge of these latter depends 
much that is fundamental both in prognosis and treatment. 
An etiologic diagnosis has, of course, an additional value in 
the matter of the prevention of heart disease, about which 
to-day the medical profession is increasingly concerned. 

The following is suggested as a tentative classification 
which emphasizes, according to their relative importance, 
the etiology, functional condition, and structural change of 
the various heart affections. 

I. TYPES OF HEART DISEASE (ETIOLOGIC) 

1. Rheumatic heart disease. 

2. Septic heart disease. (This is closely related to 
rheumatic heart disease.) 

3. Cardiovascular syphilis. 

4. Arteriosclerotic heart disease. 

5. Hypertensive heart disease. 

6. The heart in hyperthyroidism. 

7. The heart in diphtheria. 

8. Congenital heart disease. 

9. Effort syndrome: irritable heart. This is not true 
heart disease. 

10. Rare conditions. In this group should be consid- 

91 


92 


MODERN CONCEPTION OF HEART DISEASE 


ered cardiac tumors, the heart in obesity, the heart in 
severe anemia, the beer heart, and perhaps some of the 
rarer infections, etc. 

It is admitted that the causation of some of the above 
listed types of heart affections is as yet unknown, but it 
is, nevertheless, believed that an individual case will be 
more clearly understood and often more intelligently 
treated if the diagnosis includes the type to which the case 
belongs. When there exists a wholesome doubt of the 
etiologic diagnosis, this should be so stated, as such action 
will serve to stimulate further study of the patient, per¬ 
haps with eventual success. 

In many instances it is also desirable to state whether 
the cardiac affection is active or inactive, or to indicate 
that the point is not yet determined. 

II. THE FUNCTIONAL CONDITIONS 

1. Heart failure. 

a. Congestive type. 

b. Angina pectoris. 

2. The arrhythmias, or disordered heart action. 

a. Sinus arrhvthmia. 

b. Sino-auricular block. 

c. Premature beats (extrasystoles). 

(1) Auricular. 

(2) Ventricular. 

(3) Nodal. 

d. Paroxysmal tachycardia. 

(1) Auricular. 

(2) Ventricular. 

(3) Nodal. 

e. Auricular flutter. 


93 


THE CLASSIFICATION OF HEART DISEASE 

f. Auricular fibrillation. 

g. Heart-block. 

(1) Auriculo-ventricular. 

(2) Intraventricular. 

h. Atrio-ventricular rhythm and ventricular escape. 

i. Pulsus alternans. 

3. Ability to work. 

This has been classified by the New York Associa¬ 
tion of Cardiac Clinics as follows:— 

a. Able to carry on the patient’s usual activities. 

b. Able to carry on slightly to moderately curtailed 

activity. 

c. Able to carry on only greatly diminished activity. 

d. Unable to carry on any activity (without 

distress). 

III. STRUCTURAL LESIONS 

1. Endocardial. 

a. Insufficiency or stenosis (or both) of any one or 
more of the heart valves. 

2. Myocardial. 

a. Myocarditis (permissible only exceptionally, as 

part of a clinical diagnosis). 

b. Enlargement. This includes hypertrophy and 

dilatation. 

c. Ventricular preponderance. 

d. Septal defects (in congenital heart disease). 

3. Pericardial. 

a. Acute fibrinous pericarditis. 

b. Pericardial effusion. 

(1) Serofibrinous. 

(2) Purulent. 


94 


MODERN CONCEPTION OF HEART DISEASE 


(3) Hydropericardium. 

c. Adhesive pericarditis (including the obliterative 

form). 

d. Pneumopericardium and other rare forms. 

4. Position of heart. 

a. Congenital dextrocardia. 

b. Acquired dextrocardia. 

5. Great vessels. 

a. Aorta. 

(1) Dilatation. 

(2) Aneurism. 

(3) Aortitis. 

(4) Congenital changes (coarctation, trans¬ 

position with pulmonary artery, etc.). 

b. Patent ductus arteriosus. 

The following examples illustrate how the above classi¬ 
fication may be applied in the diagnosis of individual cases. 

Case 1 .—Rheumatic heart disease (inactive), auricular 
fibrillation (able to carry on only greatly diminished activ¬ 
ity), mitral stenosis, and regurgitation. 

Case 2. —Hypertensive heart disease, pulsus alternans, 
(unable to carry on any activity), cardiac enlargement. 

Study of the above suggested classification will disclose 
a number of imperfections, and yet the writer feels that its 
advantages outweigh the limitations. A very similar 
classification is in use at some of the cardiac clinics of 
Boston. Some of the rarer conditions are not listed, but 
in most instances their position in the above classification 
would be obvious; conditions which are not likely to be 
diagnosed in life are largely omitted. Only the more im¬ 
portant of the conditions represented in the above classi¬ 
fication will be discussed in this short treatise. 


SECTION II 


TYPES OF HEART DISEASE 








CHAPTER VII 


RHEUMATIC HEART DISEASE 

Rheumatic heart disease is the term which, in the 
opinion of the writer, may be advantageously applied to 
the group of conditions known as; acute or chronic endo¬ 
carditis, acute pericarditis, mitral stenosis and regurgita¬ 
tion, etc. The primary condition is a rheumatic infection 
of the heart, and the other terms, it will be seen, are but 
individual manifestations of the same infection. Such 
terms as endocarditis and mitral stenosis are open to the 
objection that they put a false emphasis on the endocardial 
or valvular changes, whereas Mackenzie has pointed out 
that, in addition, the myocardium is practically always 
involved, and on the extent of its impairment depends the 
future efficiency of the heart. 

Etiology. —Rheumatic heart disease was formerly 
held by some to be bacteria-free, but that it is an infection 
is now generally conceded; there is less agreement as to the 
identity of the invading organism. The disease would 
appear to be a modified septicopyemia. 

Rheumatic heart disease is a frequent sequela of acute 
articular rheumatism, chorea, and tonsillitis. Other condi¬ 
tions whose etiological significance seems established are, 
scarlet fever, puerperal sepsis, measles, and foci of infec¬ 
tion such as abscesses at the apex of the teeth, infections of 
the nasal sinuses, etc. Rheumatic heart disease, however, 
may be present even though there is no history of an eti¬ 
ological infection. 

7 


97 



Courtesy of Frank B. Mallory 


Plate 2. Rheumatic heart disease; acute infectious lesion of a branch of the coronary 
artery with surrounding myocarditis. 


» 



RHEUMATIC HEART DISEASE 


99 


contraction of scar tissue, and thus impede proper 
valve closure. 

A serous inflammation of the pericardium is common, 
and the formation of fibrous adhesions between the parietal 
and visceral pericardium is a frequent sequela. 

Symptoms. —In rheumatic heart disease there may be 
practically no symptoms, or those indicating slight to severe 
cardiac failure may be present. Symptoms, when present, 
do not directly indicate a rheumatic heart infection, but 
merely the presence of cardiac failure, the causation of 
which is to be determined. 

The clinical picture will vary considerably in accordance 
with whether the process is active or inactive. The pres¬ 
ence or absence of fever is the most important evidence on 
which to judge if the rheumatic heart disease is active. In 
the less acute cases, the fever may be detected only by 
the keeping of the temperature record over a period of 
several days. The minimum figure at which fever may 
be said to be present is, of course, a matter of judgment in 
an individual case. Perhaps 99.4° to 99.5° is a reasonable 
level at or above which fever may be said to be present. 

If the disease, held to be the cause, is still present, it 
is reasonable to consider the cardiac process as active. 
Following an acute attack, it seems wiser to continue to 
treat the case as active until fever and symptoms have been 
absent for some weeks. A progression in the physical 
signs usually indicates that the infection is still alive in 
the heart. On this point, however, due allowance must 
be made for the result of contraction of the damaged tissues 
after fibrosis has occurred, such as, for example, the appear¬ 
ance of the findings of stenosis of the mitral valve some 
few months after an acute cardiac infection in which the 


100 MODERN CONCEPTION OF HEART DISEASE 


mitral valve was involved with resulting insufficiency. 
The belief is now rapidly gaining ground that broken com¬ 
pensation, or to use a preferable term, an attack of heart 
failure, is nearly always a matter of infection. 

Since the term rheumatic heart disease is applied to 
hearts differing considerably in physical findings and in 
the associated symptoms, it may make the description 
clearer to build it around certain clinical types of rheumatic 
heart disease. 

Acute Rheumatic Heart Disease occurs preponder- 
atingly in the young. During the course of, or shortly after, 
an attack of rheumatic fever, or one of the other infections 
already mentioned as being associated with a rheumatic 
infection of the heart, examination may show a systolic 
murmur at the apex with perhaps a weakening of the first 
heart sound, an acceleration of the rate, and a slight en¬ 
largement of the area of dulness. One to several degrees 
of fever accompanies the above. Since the fever may be 
due to the primary disease and the cardiac signs indicate 
merely a weakening of the myocardium resulting from 
cloudy swelling, it is not possible to be certain at once if 
a true infection of the heart has taken place. Unless some 
more positive cardiac sign appears, a decision in favor of 
rheumatic heart infection is unsafe imtil there is evidence 
of persistent enlargement of the heart. 

The detection of a diastolic murmur at the aortic area, 
or along the left border of the sternum, or both, which may 
or may not mask the second sound, may, on the contrary, 
be taken as reliable evidence of infection of the heart, as 
a yielding of the aortic ring from muscular weakness is 
very rare. 

If the heart is auscultated at frequent intervals, a peri- 


RHEUMATIC HEART DISEASE 


101 


cardial rub may sometimes be heard. Pericardial friction 
is usually accompanied by precordial pain, often intense, 
and not infrequently there will be dyspnoea in addition. 
In not a few cases, the development of effusion into the 
pericardium may be observed. It should be remembered 
that the pericardial friction sound may remain over the 
base and front of the heart even in the presence of a consid¬ 
erable pericardial effusion, as the fluid tends to gravitate 
to the posterior and inferior parts of the pericardial cavity. 
Effusion into the pleural cavity is often associated with 
the pericardial effusion and occasionally the peritoneum 
may be involved in addition. 

Small nodules about the size of a pea may be palpable 
in the subcutaneous tissues and along the tendon sheaths 
of the forearms, especially on the flexor aspect. They 
appear, as a rule, early in the disease and tend to disappear 
by resolution within a few weeks after the cessation of the 
acute infection. Since they are usually painless their pres¬ 
ence will not be noted unless a deliberate search is made 
for them. 

Many of the above changes, due to acute rheumatic 
heart disease, may occur without their presence being noted, 
as the symptoms are sometimes slight and the heart, 
therefore, not examined. This very fact is a strong reason 
why the heart should be repeatedly and carefully examined 
in any patient suffering from an affection of the “rheu¬ 
matic group.” 

There is a less common type of acute rheumatic heart 
disease, in which the infection is more severe and the proc¬ 
ess of a fulminating character. It is best considered as 
an acute rheumatic carditis. The patient appears truly 
ill, and usually suffers from an increasing amount of heart 


102 MODERN CONCEPTION OF HEART DISEASE 


failure, with a fatal termination in one to three weeks. 
The fever and pulse rate are high, while the area of cardiac 
dulness tends to broaden as the heart muscle yields to the 
massive infection. Both endocardial and pericardial mur¬ 
murs may be present. 

Chronic and Recurrent Rheumatic Heart Dis¬ 
ease. —As a result of a previous acute rheumatic infection 
of the heart, the latter may present evidence of a healing of 
the process by fibrosis, or may, from time to time, be sub¬ 
ject to further attacks of rheumatic infection. The healed 
condition may well be considered as being accomplished by 
a process of scar formation which may be manifest mainly 
by physical signs and usually by some degree of diminution 
of the exercise tolerance. The less fortunate will show some 
or all the evidence of activity described in the earlier part 
of this chapter. There is considerable analogy to chronic 
tuberculosis with its residue of abnormal physical signs in 
the lung, and the tendency of the process to flare up when 
occasion favors. It has already been stated that it is often 
difficult to decide if the rheumatic heart infection is active 
or inactive, and no sharp line can be drawn between the two 
conditions. For this reason, the remaining description 
will be based on structural changes in the heart, leaving the 
decision as to the activity of the infection to be determined 
in the individual case. The author would again emphasize, 
that though it may be convenient to describe lesions of an 
individual anatomical structure, as the endocardium, the 
rheumatic infection in the same case involves the myo¬ 
cardium, and not infrequently the pericardium, in addition. 

Mitral Regurgitation. —An apical murmur occur¬ 
ring with, and usually following, the first sound, if accom¬ 
panied with evidence of cardiac enlargement, indicates an 


RHEUMATIC HEART DISEASE 


103 


insufficiency of the mitral valve, such as results from dam¬ 
age to the valve from rheumatic infection. A systolic 
murmur, completely masking the first sound, is generally 
reliable evidence of organic mitral regurgitation, but it is 
a good rule to hold that an apical systolic murmur, what¬ 
ever its transmission or quality, is insufficient evidence of 
organic mitral regurgitation unless in addition there is 
evidence of cardiac enlargement of persistent type. There 
is usually an accentuation of the second sound at the pul¬ 
monic area, but this sign is of uncertain value. A history 
of the occurrence of a disease known to be followed fre¬ 
quently by rheumatic heart disease is helpful, but the latter 
may exist though the previous history be negative. 

Mitral Stenosis. —A stenotic change of the mitral 
valve produces a typical picture of rheumatic heart dis¬ 
ease. The detection of the signs of mitral stenosis is pre¬ 
sumptive evidence of a rheumatic infection of the heart, 
for though it has been advanced by Allen 3 and others, that 
syphilis may also cause this change of the valve, it is cer¬ 
tainly a rare occurrence and supported by evidence which is 
questioned by many. To a mild degree mitral stenosis may 
occur in advanced senile arteriosclerosis. Since the devel¬ 
opment of fibrosis, and the subsequent contraction thereof, 
is necessary before the inflammatory process in the endo¬ 
cardium can cause a narrowing of the mitral orifice, it is 
quite understandable why evidence of mitral stenosis does 
not appear until several months after the acute infection 
of the heart. There is a particular value in the diagnosis 
of mitral stenosis, due to the fact that an infection severe 
enough to cause eventual obstructive changes in the valve 
also involves the myocardium to a considerable extent. 


3 Allen, H. B.: Intercol. Med. Jour, of Australas., xiv: 113 (March, 1909). 




104 MODERN CONCEPTION OF HEART DISEASE 


The myocardial damage associated with mitral stenosis is 
usually great enough to definitely impair the cardiac effi¬ 
ciency. Twenty-five to fifty per cent, of the cases of 
auricular fibrillation occur in hearts affected with stenosis 
of the mitral valve. 

Considerable confusion exists in the literature as to the 
physical signs which may be present in mitral stenosis. 
For this, and the reasons noted above, the matter will be 
given a little more attention. 

Inspection. —There is a facies which is suggestive of 
mitral stenosis. The face appears a little drawn and there 
is often a flush, sometimes cyanotic, over the cheek bones, 
with an underlying sallowness, almost a jaundice. This 
facies occurs usually only in advanced cases. Cyanosis 
may be present in the lips and ears, or more generally. 
The patient is often undernourished in type and the hands 
and feet are frequently cold. Some clubbing of the 
fingers is common in patients in whom the disease started 
in childhood. 

The apex impulse, if visible, is usually in the fifth inter¬ 
space, at or near the midclavicular line if the mitral stenosis 
is uncomplicated. If the heart is considerably hyper¬ 
trophied it may extend nearly to the anterior axillary fine, 
and with extreme preponderant hypertrophy of the right 
ventricle there may even be a systolic apical retraction in the 
sixth or seventh interspace well toward or into the axilla. 
Unusual epigastric pulsation may be found in cases of verti¬ 
cal or “drop” heart (so-called cardioptosis) and of very 
large forceful hearts, due to any cause, as well as in chronic 
mitral stenosis, so that the sign cannot be taken as evidence 
of right ventricular hypertrophy. 

Palpation over the apex usually locates the impulse 
in the fifth interspace at or near the left midclavicular line, 


RHEUMATIC HEART DISEASE 


105 


but further out and down if the heart is much enlarged. 
The quality of the impulse varies according to the size, 
strength, and excitability of the heart, hut is rarely heaving 
or prolonged. 

A thrill may accompany the apex impulse. In many 
cases it may be absent and, when present, varies from a 
mere vibration to a definite purring thrill. It is of no 
diagnostic value unless well-marked; then it points strongly 
to the presence of mitral stenosis. But when the thrill is 
well-marked and diastolic in time, it will be found that the 
other evidences of stenosis of the mitral valve are unmis¬ 
takable. I have never found the thrill of value in a doubt¬ 
ful case of mitral stenosis. 

The pulse is not of much assistance in the diagnosis of 
mitral stenosis. In a typical case it tends to show a pulse 
pressure of but slight or moderate degree. In rhythm the 
mitral pulse is not characteristic; absolute arrhythmia is 
present if auricular fibrillation has ensued as a complica¬ 
tion. When aortic regurgitation and mitral stenosis are 
associated, the latter lesion tends to limit the Corrigan 
quality of the pulse, i.e., the pulse pressure is lower than 
in uncomplicated aortic regurgitation. 

Percussion demonstrates the cardiac apex to be in nor¬ 
mal position, or if enlargement of the heart is present, the 
border of dulness generally extends laterally rather than 
downward. If the convexity of the curve of cardiac dul¬ 
ness in the left second, third, fourth, and fifth interspaces 
is outward, the presence of a lesion of the mitral valve 
becomes increasingly probable. This is, of course, merely 
evidence of prominence of the left auricle, which is more 
accurately determined by the Rontgen examination. In¬ 
crease of the percussion border to the right of the sternum 
indicates increase in size of the right auricle. Such a con- 


106 MODERN CONCEPTION OF HEART DISEASE 

dition is not uncommon in mitral stenosis when auricular 
fibrillation is present, but inasmuch as such enlargement 
can occur with the auricular fibrillation associated with 
other types of heart disease, or when a pericardial effusion 
exists, the finding is not of definite value. 

Some impairment of resonance of the apex of the left 
lung, presumably due to pressure of the dilated left auricle, 
may sometimes be noted. When this is associated with 
hemoptysis confusion has arisen as to the presence of pul¬ 
monary tuberculosis. 

Nature and cause of the murmur .—The murmur of 
mitral stenosis is caused by vibrations in the stream of 
blood flowing from the left auricle to the left ventricle. 
If the valve is narrowed to the extent that there is some 
degree of obstruction to the blood stream, the conditions 
are right for the formation of a veine fluide or jet, and the 
vibrations of this are picked up by the surrounding struc¬ 
tures, i.e. } the valve flaps, chordae tendinea?, papillary mus¬ 
cles, etc. When these structures vibrate with sufficient 
intensity, a sound is produced, which, like all sounds, is 
transmitted in all directions and is subject to refraction 
as it passes through structures differing in density. The 
sound, if of sufficient intensity, will, after being subjected 
to the influences just mentioned, be audible as a murmur 
in the stethoscope on the chest wall. 

Like all heart murmurs, the character of the murmur 
of mitral stenosis is directly dependent upon the size of 
the aperture and the velocity of the blood passing through 
it. The velocity of the auriculo-ventricular blood stream 
is determined by the difference in pressure in the two cav- 


RHEUMATIC HEART DISEASE 


107 


ities. Modern physiology 4 has demonstrated that in early 
diastole the intraventricular pressure falls to zero but not 
below it, whereas that obtaining in the left auricle is esti¬ 
mated to reach a maximum of two 5 to fifteen 6 mm. of 
mercury. When these low pressures are recalled, it be¬ 
comes quite intelligible why the murmurs of mitral stenosis 
are so often faint and of a low pitch. Furthermore, studies 
of the intra-auricular pressure curve show one high peak 
at the beginning of diastole, when the auricle contains 
the maximum content of blood, and another at the 
end of diastole or presystole, at the time of auricular 
contraction. The work of Yandell Henderson 7 makes 
it evident that the movement of blood from the left 
auricle to the left ventricle is greatest immediately after 
the auriculo-ventricular valves open, and that in hearts 
beating at a slow rhythm, ventricular filling may be prac¬ 
tically complete by the time of auricular contraction. In 
such cases auricular systole moves but a trifling amount of 
blood through the valve. 

In conformity with the above facts, it is found that the 
murmur of mitral stenosis is most often audible in diastole, 
immediately following the second sound. From there it 
may taper off in a diminuendo fashion, or continue through¬ 
out diastole, with, at times, a presystolic accentuation at 
the time of auricular contraction. The occurrence of a 
presystolic murmur, not preceded by a murmur earlier in 
diastole, is a rarity. In the experience of the writer, it is 

4 Starling, E. H.: Principles of Human Physiology, Lea and Febiger, 
1920, p. 946. 

5 Porter, W. T.: Jour. Physiol., 13: 513, 1892. 

6 Burton-Opitz, R.: Text-Book of Physiology, Philadelphia, W. B. 
Saunders Co., 1920, p. 300. 

7 Henderson, Yandell: Amer. Jour. Physiol., 16:353, 1906. 



108 MODERN CONCEPTION OF HEART DISEASE 


common to confuse the true presystolic murmur, due to 
auricular systole, with the louder crescendo murmur of 
early systole . 8 The latter murmur is produced by a stream 
of blood regurgitating through the mitral orifice during the 
early part of the contraction of the ventricle, and differs 
from the true presystolic murmur in quality, time, absence 
of a pause between it and the succeeding sound or murmur, 
and its occasional persistence when fibrillation of the auri¬ 
cles is present . 9 The crescendo, early systolic murmur, it 
is true, is often present with mitral stenosis, but it may 
exist in cases in which the autopsy demonstrates no stenotic 
change in the valve. It is safer to rely on the murmurs of 
true diastole. They are usually heard only over a small 
area near the apex, generally at the point of maximum 
impulse or internal to it. At times the sound produced 
by the blood passing through the stenosed mitral valve may 
be described as a roll or rumble, rather than a murmur. 

The first sound at the apex commonly has a quality 
described as sharp and snappy, and when of this character, 
should arouse the suspicion of the presence of mitral ste¬ 
nosis. If cardiac failure is present, or if there is a loud 
systolic murmur of mitral regurgitation masking the first 
sound, then this sound will not, of course, display the 
accentuation so often present in mitral stenosis. 

The second sound at the base may be faint, or at the 
apex, absent; but it is usually accentuated over the pul¬ 
monic area. As mentioned in an earlier chapter, too much 
weight should not be put on the diagnostic value of accentu¬ 
ation of the pulmonic second sound. 

8 Reid, W. D.: “The First Heart Sound and the Presystolic Murmur,” 
Jour. Amer. Med. Assn., 76:432 (Feb. 12, 1921). 

9 Reid, W. D.: “The So-Called Presystolic Murmur,” Jour. Amer. Med. 
Assn., 77, 21:1648 (Nov. 19, 1921). 



RHEUMATIC HEART DISEASE 


109 


Reduplication of the second sound is common in the 
mitral stenotic heart; that of the first sound is less frequent. 
It is possible that some cases of apparent reduplication of 
the second sound may be due to the occurrence of an 
abnormally loud protodiastolic third heart sound. In 
mitral stenosis this third heart sound is frequently very 
distinct. According to the late Austin Flint, “It is appar¬ 
ently due to the sudden tension on the edges of the mitral 
valve when, with ventricular diastole, it starts to open 
widely, but cannot. It may well be compared to the open¬ 
ing of a door protected by a chain latch; and the name 
‘opening snap’ is well chosen .” 10 

The Graham Steell murmur in cases of mitral stenosis 
is, in the experience of the writer, relatively uncommon, 
though some authors have stated that it is often present. 
Graham Steell, himself, reported it as a rare murmur . * 11 
It is an early, high-pitched, diastolic murmur, best heard 
at the third left costal cartilage, and is generally thought 
to be due to functional regurgitation through the pulmo¬ 
nary valve, due to increased pressure in the pulmonary 
artery. It is to be distinguished from the murmur of 
aortic regurgitation, although its time, position, and qual¬ 
ity are apparently identical. The distinction rests on the 
blood pressure and pulse findings, which in the case of 
aortic regurgitation are usually those of the Corrigan 
pulse, and on the X-ray and electrocardiographic findings, 
which are those of right ventricular hypertrophy if the mur¬ 
mur is a Graham Steell. A difference of opinion exists 

10 Flint, Austin: A Manual of Physical Diagnosis, 8th edition, revised 
by Henry C. Thacher, Lea and Febiger, 1920, p. 311. 

11 Steell, Graham: “The Auscultatory Signs, etc., of Mitral Stenosis: 
A Statistical Enquiry,” Med. Chron., Manchester, 1895, iii (N. S.), 409. 
“Mitral Stenosis,” Internat. Clin., 1898, iii (8th series), 1411. 



110 MODERN CONCEPTION OF HEART DISEASE 

as regards the frequency of this murmur; it seems likely 
that it is sometimes said to be present when the true condi¬ 
tion is aortic regurgitation, associated with mitral stenosis. 

The history may disclose embolic infarction to the brain 
or elsewhere and at times hemoptysis. Both of these may 
be due solely to mitral stenosis and call for careful examina¬ 
tion of the heart. The mechanism of the production of 
this embolism is quite simple. In the dilated condition of 
the auricle, often found in mitral stenosis, especially where 
co-ordinate contraction of the auricle has ceased, as in 
auricular fibrillation, thrombosis is common. Bits of the 
thrombus or thrombi are apt to be loosened and directed 
into the blood stream of the pulmonary circulation in case 
the embolus comes from a right auricular thrombus, or 
the systemic circulation (particularly brain and kidneys), 
if the left auricle is involved. More rarely aphonia, from 
paralysis of the left recurrent laryngeal nerve, is caused by 
mitral stenosis. 

X-Ray.—B ontgen evidence consists mainly in the 
demonstration of the “mitral shaped heart,” in which the 
organ appears more rounded than normally. The enlarge¬ 
ment is lateral, and particularly in the region of the auricles. 

Electrocardiogram .—The “typical” tracing may show 
the auricular or P wave over 3 mm. in height or more than 
0.1 second in duration, which is evidence of auricular hyper¬ 
trophy, and the latter is most commonly found in mitral 
stenosis. The tracing may also yield evidence of right 
ventricular preponderance. The absence of both of these 
changes does not disprove the presence of mitral stenosis, 
inasmuch as it is only the chronic advanced cases of uncom¬ 
plicated mitral stenosis that give the “typical” electro¬ 
cardiogram. In other words, if the electrocardiogram 


RHEUMATIC HEART DISEASE 


111 


shows these findings it is fairly certain that mitral stenosis 
is present; if it does not, it is of no help. Of course, if 
the auricles are fibrillating the P wave will be absent. 

Aortic regurgitation may also occur in rheumatic heart 
disease. Steell 12 found some change, though often trivial, 
in the aortic valve in 50 per cent, of his cases of mitral 
stenosis which were subjected to autopsy. Since insuffi¬ 
ciency of the aortic valve is not confined to rheumatic heart 
disease, but is even more common in cardiovascular syphilis, 
and the physical signs are essentially the same in the two 
affections, the further discussion of this valve lesion will 
be deferred. 

Aortic stenosis is an infrequent complication of rheu¬ 
matic heart disease. It is a relatively rare valvular lesion, 
and when present the aortic valve is usually insufficient in 
addition. Though the rheumatic type of heart infection 
is practically the sole cause of a stenotic change in the 
aortic valve, for purposes of convenience its further descrip¬ 
tion will be postponed to a later chapter. 

Adhesive pericarditis may result from organization of 
the exudate of the acute pericarditis. It is frequently 
present to some degree without causing signs or symp¬ 
toms 13 by which it may be diagnosed. If the adhesions 
extend to the adjacent structures there is more likelihood 
that abnormal physical signs may result. A systolic re¬ 
traction of the chest wall at the base of the left axilla and 
in the region of the eleventh and twelfth ribs in the back 

12 Steell, Graham: Med. Chronicle, 3: 409, 1895. 

13 In a study of 15 cases at the Massachusetts General Hospital, in which 
at autopsy the pericardial sac was found obliterated in 7 and united by 
numerous fibrous adhesions in the remaining 8, the condition was diagnosed 
in life in but two instances. Reid, W. D.: Boston Med. and Surg. Jour., 
clxxxiii, 13:386 (Sept. 23, 1920). 




112 MODERN CONCEPTION OF HEART DISEASE 


(Broadbent’s sign), if present, strongly suggests adhesions 
of the pericardium to the diaphragm. If pleural adhesions 
complicate, Litten’s sign of the excursion of the diaphragm 
and the respiratory excursion of the base of the lungs, 
may be abolished. Adhesions to the mediastinum may 
fix the position of the apex impulse so that it does not show 
the normal shifting with change of position. At times 
this tendency of fixation of the heart and adjacent struc¬ 
tures may be more clearly appreciated by examination 
under the fluoroscope. 

It should be emphasized that a systolic retraction visible 
at the apex and between it and the sternum should not be 
interpreted as due to adhesions of the pericardium. Such 
a phenomenon has been demonstrated by Mackenzie and 
others to be produced by hypertrophy of the right ventricle. 
Diminution or obliteration of the arterial pulse with inspi¬ 
ration (the paradoxical pulse), if present, is not of diag¬ 
nostic value, since it is present in many normal individuals. 
Diastolic collapse of the cervical veins, noted by Fried¬ 
reich, is likewise of uncertain value as an indication of 
pericardial adhesions, since it is now known to be a feature 
of the ventricular form of venous pulse, occurring in 
auricular fibrillation, etc. 

Although the heart is frequently of normal size in the 
presence of adhesive pericarditis, it may be considerably 
enlarged, and therefore cardiac hypertrophy, out of pro¬ 
portion to or not explained by other lesions, is suggestive 
of pericardial adhesions. A few cases are seen in which a 
change from the upright posture is promptly followed by 
cyanosis and dyspnoea. 

In the majority of cases, it is repeated, pericardial 
adhesions will escape recognition in life. This seems of 


RHEUMATIC HEART DISEASE 


113 


less importance since myocardial and endocardial damage 
are usually present in the same case and a diagnosis of 
rheumatic heart disease may yet be made. 

Various arrhythmias, such as auricular fibrillation and 
heart-block, and, occasionally, the rarer condition, auricu¬ 
lar flutter, may occur in the acute stage of rheumatic heart 
disease, but are more common when the infection may be 
said to be old or chronic. Their discussion will be deferred. 

Diagnosis. —The day has passed when it is sufficient 
to diagnose any of the structural lesions noted above; to¬ 
day the physician is expected to go further and attempt 
to determine the underlying cause. Familiarity with the 
facts already briefly mentioned will usually lead to the 
correct conclusion. A careful history is often of great 
assistance. In fact, every patient who is at present ill 
with or who has previously suffered from any of the dis¬ 
eases mentioned under etiology should be considered as a 
case of potential rheumatic heart disease until careful 
examination and the lapse of a sufficient time has proved 
otherwise. During the acute and subacute stage of the 
“rheumatic group” of infections, the heart should be 
examined repeatedly. 

Evidence of cardiac enlargement, not otherwise ex¬ 
plained, gives strong support for a diagnosis of rheumatic 
heart infection. Mitral stenosis is practically always of 
rheumatic origin. The same may be said of stenosis of 
the aortic valve, but the value of the diagnosis of this lesion 
is comparatively slight, since it is known that obstructive 
changes in the aortic cusps are relatively rare, and it is 
notorious that the clinical diagnosis is frequently uncon¬ 
firmed at autopsy. Aortic regurgitation may be rheu- 


8 


114 MODERN CONCEPTION OF HEART DISEASE 


matic but in patients over twenty years of age it is safer to 
first suspect a syphilitic origin. Pericardial effusion is 
usually good evidence of rheumatic heart disease. Peri¬ 
cardial adhesions, which cause sufficient signs and symp¬ 
toms to be diagnosed in life, may likewise be attributed to 
a rheumatic infection of the heart; tuberculosis also causes 
adhesive pericarditis, but in the experience of the writer 
the condition is usually recognized only at autopsy. 

Further discussion of the diagnosis of rheumatic heart 
disease may well be dismissed, after emphasizing that the 
evidence of its presence should be checked by a complete 
examination of the j)atient and the absence of the findings 
of one of the other types of heart disease. 

Prognosis. —The prognosis of rheumatic heart disease 
may be said to be a matter of infection. The severity of 
the initial attack, the amount of myocardial damage in¬ 
curred, and the continuance or recurrence of the infection 
are all important. 

If the initial attack is attended with a high fever and 
marked evidence of cardiac embarrassment, death mav 
result within one to several weeks. The great majority 
of cases, however, are not ushered in with such severity, 
and the future depends upon the amount of damage caused 
by the first attack and especially upon the recurrence of 
the infection in the heart. If the case is well treated by 
rest and if success attends the modern method of prevent¬ 
ing recurrence by removal of the foci of infection, such 
as the tonsils, etc., a useful heart may often be retained. 
The prognosis should, therefore, usually be hopeful but 
guarded. Some degree of limitation of the exercise tol¬ 
erance is the rule. 


RHEUMATIC HEART DISEASE 


115 


Pericarditis, and even an extensive pericardial effusion, 
is not necessarily of bad import. It is surprising to see 
the frequent recovery from even a large effusion into 
the pericardium. 

If mitral regurgitation is the sole evidence of the rheu¬ 
matic infection, provided sufficient time has elapsed to 
preclude the appearance of stenosis of the same valve, the 
heart may well be considered to have suffered but slight 
damage, for it has been shown that in such hearts the myo¬ 
cardium, the all-important structure, is but little impaired. 

Mitral stenosis and aortic regurgitation are much more 
important, for in these cases it may be assumed that the 
infection has been of sufficient severity to cause material 
damage to the myocardium. Auricular fibrillation is a 
common sequela, especially of the former lesion. Little 
weight can be placed upon aortic stenosis, as its diagnosis 
is too unreliable. 

Heart-block, auricular fibrillation, and auricular flutter 
are all serious complications. 

Treatment. —Rest in bed .—All cases of acute rheu¬ 
matic heart disease should be put to bed and kept there 
for weeks or months. How long will depend upon the 
severity and duration of the acute attack. If fever has 
been present but a few days and the sole evidence of cardiac 
infection is the appearance of an apical systolic murmur, 
it should usually be safe to permit the patient to get out of 
bed gradually, after the temperature and pulse rate have 
been normal one to two weeks. A marked elevation of 
the heart rate, or symptoms of cardiac embarrassment on 
change of posture, indicate that the heart has not yet 
sufficiently recovered, and further rest should be prescribed. 


116 MODERN CONCEPTION OF HEART DISEASE 


Those patients in whom the fever lasted for more than 
about a week (due allowance, of course, being made for 
fever which may properly be considered non-cardiac in 
origin), and in whom the development of the more serious 
changes, such as aortic insufficiency, pericardial effusion, 
auricular fibrillation, or heart-block, may have been ob¬ 
served, clearly demand absolute rest for one to several 
months. It takes time for the heart muscle to undergo 
the maximum repair for the damage incurred. 

Decision as to the need of rest in bed in a case of 
chronic rheumatic heart disease should be based upon the 
activity or non-activity of the infection. Absolute rest is 
desirable for a period long enough to permit healing of 
the cardiac damage recently acquired. Since many of the 
physical signs may be due to lesions previously produced 
and healed by scars, it is usually permissible to let the 
patient up sooner than if it were known that the heart 
infection is all of recent origin. The propriety of allow¬ 
ing the patient to cease rest in bed is to be checked as 
suggested above, in the discussion of the treatment of cases 
of acute rheumatic heart disease. 

In chronic cases and all those in which there is no evi¬ 
dence of present or recent activity of the infection in the 
heart, rest is not indicated. Restriction of the patient to 
bed should be prescribed only in case the process in the 
heart is active or there is a reasonable suspicion thereof 
(it being recalled that there is a growing belief that there 
is some degree of infection in most cases of heart failure). 

Removal of the focus of infection .—A serious attempt 
should be made in each case to determine, and if possible 
remove, the focus from which the infection travelled to 


RHEUMATIC HEART DISEASE 


117 


the heart. Most frequently tonsillectomy is the needed 
procedure. This is best done shortly after the acute attack. 
In some cases, the recurrence of acute attacks may make it 
unwise to delay further with the removal of the focus, 
if known. 

Something should be said about the attitude of the 
physician and patient to the operative procedure, ton¬ 
sillectomy, for example. If the removal of the tonsils is 
proposed as a cure for rheumatic heart disease, or as an 
absolutely certain preventive of further cardiac infection, 
disappointment will frequently result. But if the physi¬ 
cian explains that an infection is the cause of the existing 
trouble in the heart, that the prevention of further infection 
is all-important, and that the best prospect of accomplish¬ 
ing this lies in the removal of the primary focus, in this 
case the tonsils, the purpose of and the probability of bene¬ 
fit resulting from the operation should be readily grasped. 
The tonsillectomy may be offered as the best kind of 
health insurance. 

After the age of forty, the need for tonsillectomy is 
less certain, as the tonsils are infrequent offenders in the 
subsequent period of life. The dental infections are then 
frequent, and it is a good rule to clean out such, even 
though there is considerable reason to believe that most of 
the active infection of rheumatic heart disease occurs 
before the age of forty years. 

Digitalis is indicated if auricular fibrillation, auricular 
flutter, or heart failure of the congestive type is present. 
Since the chief action of this drug is to produce therapeutic 
heart-block, its administration will rarely prove of value 
save in cases of accelerated rate of supraventricular origin. 


118 MODERN CONCEPTION OF HEART DISEASE 


There is considerable doubt as to the propriety of the pre¬ 
scribing of digitalis during the febrile stage. Further 
discussion of the action and usage of this specific cardiac 
drug will be postponed to a later section of this book. 

Symptomatic. —Pain, insomnia, restlessness, dyspnoea, 
and depression of spirits should be relieved. Attention 
should be directed to the care of the bowels and the diet. 
Since the treatment of the above features in rheumatic 
heart disease is essentially the same as in heart disease of 
other causation, its details will be deferred to the chapter 
on treatment. 

Regulation of the patient’s life .—When convalescence 
is well established, advice should be given as to the amount 
of exercise that may be proper for the individual patient, 
and the nature of the employment and daily routine of the 
patient’s life should be discussed. It may be stated at 
this point that in cases in which the cardiac damage results 
solely in insufficiency of the mitral valve, or even in uncom¬ 
plicated aortic regurgitation when there is but slight im¬ 
pairment of the exercise tolerance, but slight restriction 
should be imposed. In the past it appears that a mistake 
has been made in limiting too severely the exercise of this 
type of case. To avoid repetition, the reader is referred 
to later chapters for further discussion of the above, and on 
the therapy of pericardial effusion, the arrhythmias, etc. 


CHAPTER VIII 
SEPTIC HEART DISEASE 

Although this form of cardiac infection is really a 
form of rheumatic heart disease, in which the especial viru¬ 
lence of the attacking organism causes the more severe 
cardiac changes and constitutional symptoms, it seems 
justifiable, for clinical purposes, to accord it a separate 
description. It is met in the literature under the terms 
of malignant, ulcerative, or infectious endocarditis, or, 
where the causative organism has been identified, the latter 
is often used as part of the descriptive name of the disease, 
as, pneumococcic endocarditis, staphylococcic endocarditis, 
etc. None of these terms seems to the author quite satis¬ 
factory. It may be emphasized that the use of the term 
endocarditis appears objectionable, in that it creates 
the false impression that the process is limited to the 
endocardium. 

Etiology. —The etiology of septic heart disease differs 
from that of rheumatic heart disease in that the triad— 
rheumatic fever, chorea, and tonsillitis—is less prominent. 
The condition is more likely to be associated with wound 
sepsis or puerperal infection, or to follow pneumonia, 
gonorrhea, empyema, etc., but, on the other hand, the his¬ 
tory of an etiological disease is often wanting. Previous 
rheumatic or atheromatous changes in the heart are apt to 
favor the development of septic endocarditis. The com¬ 
moner causative organisms are: the streptococci, staphylo¬ 
cocci, pneumococci, and gonococci. 

Pathology. —The pathology is similar to, but more 

119 


120 MODERN CONCEPTION OF HEART DISEASE 


severe, than that of rheumatic heart disease. The process 
involves the myocardium as well as the endocardium, and 
often the pericardium also. The endocardial changes 
tend to a rather severe character; vegetations, sometimes 
of considerable size, form on the valve membranes and in 
some cases a necrosis of the tissue occurs, leading to an 
ulceration or perforation of the valve cusps. The vegeta¬ 
tions are quite friable and form a ready source of emboli. 
These emboli are loaded with organisms and thus they act 
not only in a mechanical way, but also serve as foci of 
infection where they lodge. The masses which form on 
the valves and adjacent endocardium are not well chan¬ 
nelled with blood vessels, a fact which apparently is of 
importance in understanding the failure of treatment by 
means of bactericidal serum. 

The spleen is usually enlarged and soft—the septic 
type of spleen. 

Symptoms. —The symptoms show considerable varia¬ 
tion. There is no typical clinical picture of septic heart 
disease. The majority of cases may be fitted into one of 
two groups or types. 

The acute tyye begins with violent symptoms and leads 
to a fatal end in a few days to weeks. Sometimes it may set 
in with a chill. After one or two days’ prodromes, among 
which headache, fever, and a feeling of being sore all over, 
predominate, the patient often falls quickly into a stupe¬ 
fied condition, shows high temperature, quick pulse, very 
rapid respiration, and, on skin and retina, more or less 
hemorrhages. More rarely, miliary or larger blisters, and, 
when the staphylococcus is the invading organism, pustules 
may appear on the skin. Without further local symptoms, 



Courtesy of Frank B. Mallory 

Plate 3. Large vegetations on the mitral valve, in septic heart disease due to the pneumococcus. 






SEPTIC HEART DISEASE 


121 


death ensues in the course of four to seven days, especially 
if the streptococcus or staphylococcus is the infecting agent. 

When septic heart disease complicates lobar pneu¬ 
monia, as a rule there follow, after a few (three to five) 
fever-free days, severe febrile general symptoms, which 
point to the fresh disease, and continue during the ten to 
twenty days’ duration of the affection. 

In most cases a cardiac murmur is to be heard. Occa¬ 
sionally the murmur has only a soft blowing character 
which one not uncommonly hears in other febrile diseases, 
but more often, it is loud, blowing or scraping. In not 
a few cases the murmur is entirely lacking, as in many cases 
the soft vegetations hinder neither the normal flow of 
blood nor the regular closing of the valve. 

As a result of emboli, especially in patients in whom the 
pneumococcus is the attacking organism, a panophthalmia 
may occasionally occur and still more rarely a purulent 
meningitis. Other disturbances resulting from emboli are 
abscesses in the liver, spleen, and bowel. As a result of an 
embolus lodging in the mesenteric artery, fatal intestinal 
hemorrhage has occurred. A renal abscess may develop, 
especially in the staphylococcic infection. The organism 
can be identified in the urine. 

The chronic type begins much less severely. Occa¬ 
sionally there is a sore throat, influenza, or a severe cold 
with a fever preceding, from which a proper recovery has 
not ensued. The patients feel weak, often have pains or 
twinges in the extremities, and have occasional light chills. 
In other cases these symptoms have occurred without the 
patient being aware of any preceding acute illness. The 
temperature is elevated, 100° to 102° being the average. 


122 MODERN CONCEPTION OF HEART DISEASE 


The picture may remain unchanged for a whole month. 
Occasionally chills are entirely absent, but in their stead 
are sweats, especially at night or in the early morning. 

In other cases, lasting over five or six months, in which 
the ordinary streptococcus is at work, periods of intermit¬ 
tent fever slip in; more rarely, days with a mild elevation 
of temperature and, at irregular intervals, violent chills 
occur. The cutaneous and retinal hemorrhages and spots 
in the skin are apt to appear, not all at once, but in suc¬ 
cessive crops. 

Energetic, work-loving natures lose their strength and 
take to bed. On examination at this stage there will com¬ 
monly be found characteristic heart murmurs, enlargement 
of the liver, and swelling of the spleen. Most patients of 
this class experience more or less active rheumatic pains, 
which affect the joints less severely than the adjacent mus¬ 
cular tissue or the periosteum of the long bones. In some 
instances there may be sharply circumscribed painful areas 
at the tips of the fingers. 

Fleeting effusion into the joints may take place. Also 
there follows, towards the end of life, a severe nephritis, in 
which numerous colorless red corpuscles and often masses 
of epithelial casts appear. Not uncommonly the picture 
is that of a severe hemorrhagic nephritis. 

In contradistinction to the acute form, chronic septic 
heart disease only exceptionally leads to purulent metas- 
tases. Renal and splenic infarcts are common and often 
without symptoms. Embolic processes in the brain may 
produce aphasia, hemiplegia, or convulsions, but these are 
often of a temporary nature. Gangrene of an extremity 


SEPTIC HEART DISEASE 123 

and aneurisms are further results of damage wrought 
by emboli. 

Diagnosis. —The diagnosis offers considerable diffi¬ 
culty. Septic infection of the heart should be suspected 
where there is a fever of protracted duration of an irregular 
type and associated with chills or sweats. Evidence of 
emboli, petechiae in the skin, a palpable enlargement of the 
spleen, sallowness of the complexion, some degree of 
anemia, and any of the symptoms mentioned above, point 
strongly to the presence of a septic infection of the heart. 
The diagnosis is confirmed by the finding of numerous 
colonies of the infecting organism in repeated cultures of 
the blood. Repeated blood cultures may, however, re¬ 
main sterile. 

Other diseases which may at times be simulated are: 
typhoid fever, miliary tuberculosis, malaria, other cardiac 
diseases, pneumonia, meningitis, results of emboli, uremia, 
pyelitis, diseases of the biliary tract, and acute articular 
rheumatism. Limitation of space forbids the discussion 
of all these affections. 

Typhoid fever and the miliary form of tuberculosis 
offer the greatest problem in differential diagnosis. A 
careful history and study of the symptoms and physical 
signs are essential. The laboratory findings are often the 
most successful means of differentiating these diseases. 
The white count doesn’t help much, as a leucopenia may 
occur in septic heart disease as well as in the other two 
conditions. A positive Widal reaction (unless the patient 
has had a course of the typhoid vaccines, as did the soldiers 
in the recent war) and the finding of typhoid bacilli in 
the blood culture, will establish the presence of typhoid 


124 MODERN CONCEPTION OF HEART DISEASE 


fever. Sputum and lumbar punctures may sometimes 
assist in the diagnosis of miliary tuberculosis. Blood cul¬ 
tures which are positive for organisms other than the ty¬ 
phoid bacillus prove the diagnosis of septic heart disease. 
It is suggested that the blood culture should show numerous 
colonies and that the finding should be repeated in one 
or more subsequent blood cultures, in order to rule out 
mistakes due to contamination, and errors in laboratory 
technique. 

Septicemia , it is true, may yield a positive blood culture. 
The presence of a septic wound, or evidence of puerperal 
sepsis, and the relative lack of the findings of cardiac 
involvement, are generally sufficient to establish the diag¬ 
nosis of septicemia in preference to septic heart disease, 
a similar but more localized affection. 

Prognosis. —The prognosis is almost always fatal. 
The patient gradually loses ground, with more and more 
anemia and often with increasing damage from the dis¬ 
charge of septic emboli into the blood stream. Recoveries 
exceptionally occur. 

Treatment. —The treatment. The patient should be 
at rest in bed. Fresh air and good nursing are important. 
The diet should be generous; the aim being to aid the 
patient in his fight against the infection by supplying 
plenty of nourishing food. Attention should be directed 
to the bowels and symptoms treated as they arise. 

Billings reports some success from the use of cacodylate 
of soda in a dosage of gm. 0.6 to 1.0 (gr. 10 to 15) daily 
hypodermically, and the same amount every two to three 
days intravenously. Others have used small doses of 
arsphenamine. 


SEPTIC HEART DISEASE 


125 


It would seem that some sort of specific therapy should 
offer a logical method of attack, but experience has shown 
that it is of but little avail. Vaccines are not indicated. 
The free use of bactericidal serum from a horse made 
highly immune to the organism obtained from the blood 
culture of the patient has been tried. A parent or near 
relative has been made immune in a similar fashion and 
then used as a donor for repeated blood transfusions . * 1 
As a result the organisms have disappeared from the 
patient’s blood for about twelve hours and then return in 
large numbers . 2 A probable reason is that, due to the 
lack of blood vessels in the septic focus in the heart, there 
is a failure of penetration of the bactericidal serum and the 
masses of organisms in the depths of the lesion remain 
unscathed. 

1 Levisox, L. A.: Jour. Lab. and Clin. Med., St. Louis, 4: 191 (Jan., 1921). 

1 Personal conversation with Benjamin White, Director of the Biologic 

Laboratories of the Massachusetts Board of Health. 



CHAPTER IX 

CARDIOVASCULAR SYPHILIS 

Infection of the heart and the aorta by the spirochete 
of syphilis produces one of the most important types of 
heart disease. Statistics 1 from various clinics show the 
presence of cardiovascular syphilis in 3.5 to 7 per cent, of 
the total autopsies and in 75 to 85 per cent, of the autopsies 
on bodies known to have been infected with syphilis. In 
40 of the 54 cases in which this disease was found at post¬ 
mortem examination at the Massachusetts General Hos¬ 
pital, the condition was held to be the primary cause of 
death. In three of the fourteen remaining cases, in which 
the cardiovascular syphilis was listed as a secondary cause 
of death, the process was advanced to a serious degree. 

Etiology. —As early as 1724, Lancisi , 2 according to 
Allbutt, associated “Aneurysma Gallicum” with “impure 
coitus” signs of syphilis elsewhere in the body, but it has 
been only since the discovery of the spirochete in the aortic 
wall in 1906 and 1907 by Reuta , 3 Benda , 4 and Schmorl , 5 
and in the myocardium by Warthin 0 in 1916, that the true 
nature of cardiovascular syphilis has been understood. 
The lesions are, then, due to the invasion by the spirochete 
of the tissues of the heart and aorta. 

1 Reid, W. D.: Boston Med. and Burg. Jour., clxxxiii, No. 3: 67 and 
4:105 (July 15 and 22, 1920). 

“Lancisi: “De novissime observatis abscessibus,” c, xviii, ed. 1724. 

s Reuta: Munch, med. Woch., liii: 778, 1906. 

4 Benda, C.: Berlin, klin. Wocli., xliii:989, 1906. 

“Schmoel: Munch, med. Woch., liv: 188, 1907. 

* Wabthin, A. S.: Amer. Jour. Med. Sci., cliii: 508, 1916. 

126 




(Courtesy of A. S. Warthin.) 


Fig. 26 .—Spirochetes in the myocardium. 



Courtesy of A. S. Warthin.) 


Fig. 27.—Syphilitic myocarditis. 




CARDIOVASCULAR SYPHILIS 


127 


The involvement of the heart and aorta may begin 
before or during the so-called secondary stage of syphilis. 
However, sixteen years was the average period elapsing 
between the primary lesion of the luetic infection and the 
appearance of symptoms of circulatory disease, in the cases 
treated at the Massachusetts General Hospital ; 7 the short¬ 
est was six months and the longest thirty-three years. 

Men are attacked about three times as frequently as 
women. The age period from 35 to 50 years shows the 
highest number of cases. Congenital cases are not infre¬ 
quent at the age of 15 to 20 years 8 and are well known in 
syphilitic infants. Laborious or athletic pursuits appear 
to be important determinants. Alcohol is probably unim¬ 
portant, as the disease occurs in total abstainers. 

Pathology. —In recent years there has been an appre¬ 
ciation of the fact that, coincident with the syphilitic lesion 
in the aorta, the heart proper is usually involved. To the 
naked eye, the heart may show dilatation, hypertrophy, 
atrophy, and patches of fibrosis in the wall of the left 
ventricle. In congenital cases the wall of the right ventri¬ 
cle may be chiefly affected . 9 

In many cases the fibroid changes are detected only on 
microscopic examination. To follow Warthin’s descrip¬ 
tion , 9 the essential lesion is an interstitial myocarditis, 
characterized by infiltration with lymphocytes and plasma 
cells along the vessels between the muscle fibres. The 
entire heart wall, from epicardium to endocardium, includ¬ 
ing the papillary muscles, may be involved in the infiltra- 

7 Reid, W. D.: Jour. Amer. Med. Assn., lxxiii: 1832, 1919. 

®Allbtjtt, C. A.: Diseases of the Arteries, including Angina Pectoris, 
Macmillan & Co., 1915, ii: 140. 

9 Warthix, A. S.: Amer. Jour. Syphilis, 2:425 (July, 1918). 



128 MODERN CONCEPTION OF HEART DISEASE 


tions; but in the average case they lie nearer to the 
endocardium. In the great majority there are areas of 
healing by fibrosis associated with areas in which the process 
is active. A progressive fibrosis of the heart muscle event¬ 
ually takes place in all cases. 

Sclerosis of the larger branches of the coronary arteries 
is rare, even in cases affected by angina pectoris. In the 
most severe cases there is infiltration around the smaller 
arteries. An aneurism of the wall of the left ventricle is 
not uncommon. True gummata in the myocardium are 
relatively rare. 

The aortic valves showed slight to moderate fibrous 
thickening in about two thirds of the Massachusetts Gen¬ 
eral Hospital cases, while in another ten per cent, the 
damage was more extensive. The corelation of the clinical 
and the post-mortem evidence 10 indicates that the insuffi¬ 
ciency of the aortic valve, present in 40 per cent, of the 
cases, is more often dependent upon a yielding of the 
aortic ring than upon actual damage to the valve curtains. 
Aortic stenosis is a great rarity. Syphilitic changes of the 
mitral and tricuspid valves apparently do not occur. 9,11 

There is much variation in the extent of the pathological 
changes in the arterial system. The lesions are mostly 
found in the wall of the aorta and predominatingly in the 
ascending and transverse arch. This aspect of cardio¬ 
vascular syphilis has been so evident that the disease is com¬ 
monly referred to in the literature as syphilitic aortitis. 
In 94 per cent, of the group of cases examined at the 
Massachusetts General Hospital 10 the ascending portion 

10 Reid, W. D.: Boston Med. and Surg. Jour., clxxxiii, No. 3:67 and 4:105 
(July 15 and 22, 1920). 

D Beooks, H.: Amer. Jour. Syphilis, 5, 2:217 (April, 1921). 



CARDIOVASCULAR SYPHILIS 


129 


of the arch was affected, blit not infrequently the process 
was as extensive in the transverse arch, and sometimes 
more so. 

In its acuter stages syphilitic infection of the aorta is 
not arterio-sclerotic but inflammatory; it is, strictly speak¬ 
ing, aortitis. The primary site is along the vasa vasorum 
in the adventitia; the media is soon involved and the intima 
last of all. Around the vasa vasorum are found collections 
of plasma and lymphoid cells, and, in the more acute foci, 
the treponemata may be demonstrated by the Levaditi 
silver impregnation method. A definite gumma is rare. 
There may be large areas of healing by scar. It is the 
irregular distribution of the fibrosis and the necrosis, i.e., 
the reparative and the destructive changes, which gives 
the irregular puckered appearance to the aortic wall in 
cases of advanced aortitis. The absence of calcification 
in the luetic lesion is a contrast with its prevalence in 
arteriosclerosis. Warthin 12 emphasizes that the patho¬ 
logical diagnosis of syphilis is essentially microscopic, as 
to the naked eye the tissue may appear sound. 

When the process has caused the aorta to dilate consid¬ 
erably it is often a matter of personal choice with the 
examiner whether he employs the expression syphilitic 
aortitis with dilatation or syphilitic aortitis with aneurism; 
there is no hard and fast line between the two conditions. 
Large aneurisms of the saccular or dissecting types may 
occur. These big aneurisms involve the adjacent structures 
by pressure, and by a process of erosion may penetrate 
and finally rupture with fatal hemorrhage into the peri¬ 
cardial sac, the chest wall, trachea, esophagus, etc. A 

12 Warthin, A. S.: Amer. Jour. Syphilis, 2:425 (July, 1918). 


9 



130 MODERN CONCEPTION OF HEART DISEASE 


great majority of aneurisms which involve the aorta before 
it pierces the diaphragm are due to syphilis, but rarely, 
usually of the small saccular type, they may result from 
non-luetic infections. 

Symptoms. —Cardiovascular syphilis is for the most 
part insidious. Such symptoms as occur are mainly due 
to the cardiac lesions rather than to those of the aorta, 
save for the symptoms caused by pressure when an aneu¬ 
rism has formed. It does not seem practical to classify the 
cases in relation to the anatomical lesion, but perhaps they 
may better be divided into acute or chronic according to 
the intensity of the symptoms. Tides of activity occur. 

If there be symptoms, pain is prominent. It varies 
from a sense of tightness or burning about the upper 
sternum to the utter torture of severe angina. It may 
come in attacks, be associated with exertion, or be present 
almost continuously. In location and radiation the pain 
of cardiovascular syphilis is wont to resemble that of 
angina pectoris (which see). 

Shortness of breath is common. It may be associated 
with rapid heart action and other evidence of cardiac em¬ 
barrassment. Cough and weakness are further symptoms. 

Fever of a low-grade “septic” or irregular type may 
occur, but is of little diagnostic value, as it is rare that 
careful examination of the patient fails to show the pres¬ 
ence of some other condition which might cause the rise 
in temperature. Also, of course, fever may be present 
at various times in syphilis, but does not per se indicate 
invasion of the circulatory tissues. 

In cases in which the luetic infection has seriouslv 
impaired the integrity of the heart and aorta, symptoms 


CARDIOVASCULAR SYPHILIS 


131 


consistent with advanced heart failure will be in evidence. 
When an aneurism is present pressure symptoms may arise. 
A rather strident whistling respiration on exertion, while 
by no means an initial sign, may yet long precede other 
respiratory signs as a symptom of pressure. A “brassy 
cough” and partial aphonia are frequent results of involve¬ 
ment of the left recurrent laryngeal nerve in its course 
round the arch of the aorta. The direction in which pres¬ 
sure is exerted by an aneurism and the rapidity with which 
dilation occurs and grows are undoubted determining 
factors in the production and absence of symptoms. 

Physical Signs. —The evidence of luetic infection of 
the circulation that is obtained by physical examination 
varies according to the nature and the extent of the lesions 
present. In many cases physical signs may be essentially 
absent. The discussion of the physical signs may be con¬ 
sidered to best advantage, perhaps, under inspection, pal¬ 
pation, percussion, and auscultation. 

Inspection is of value only in advanced cases. Thus, 
a visible throbbing of the carotid suggests insufficiency of 
the aortic valve, which, in most cases in adults, is known 
to be of syphilitic origin. A visible pulsation in the supra¬ 
sternal notch may mean a dilated aortic arch, Again, any 
visible pulsation in the second or third intercostal space 
suggests aneurism. Enlargement of the cervical veins 
may be noted, but should not be expected save with cases 
complicated by aneurism and with other signs of pressure. 
Inequality of the pupils from irritation of the cervical 
sympathetic nerve may occur. 

Palpation. A palpable impulse in the suprasternal 
notch, due to dilation of the arch of the aorta, is, at best, 


132 MODERN CONCEPTION OF HEART DISEASE 


not a particularly reliable sign, as it is not always present 
and also occurs in arteriosclerosis and in some other non¬ 
specific conditions. In case aortic regurgitation is present, 
the apex impulse is usually moved downward and to the 
left and accompanied by the Corrigan or collapsing type 
of pulse. An expansible pulsation, lateral to the base of 
the sternum, is strong evidence of aneurism. 

Percussion may be useful to detect enlargement of the 
first part of the aorta. The supracardiac dulness is most 
marked in the midmanubrial region, and commonly the 
dulness is greater to the right than to the left. In rare 
instances an area of dulness has been detected to the left 
of the third and fourth dorsal vertebras due to a dilation 
or aneurism of the adjacent aorta. 

Auscultation .—The second sound at the second right 
costal cartilage often is of a duller note than normal, but 
practically the same quality may occur in arteriosclerosis. 
A systolic murmur, often very faint and soft, but some¬ 
times loud and rough, at the aortic area is frequently 
present in cardiovascular syphilis, and occasionally is 
accompanied by a thrill, not necessarily indicating a ste¬ 
notic change in the aortic orifice. If the luetic infection has 
caused an insufficiency of the aortic valve, the characteristic 
diastolic murmur of aortic regurgitation will be noted. 
This, of course, may or may not mask the second sound. 
At the apex a systolic murmur due to an insufficiency of the 
mitral valve, and of muscular origin, is commonly present 
in addition to the aortic findings. And in some cases, the 
Austin Flint murmur at the apex may be a further find¬ 
ing. A friction rub over the base has been reported. 

An abnormal rhythm may control the heart. Partial 


CARDIOVASCULAR SYPHILIS 


133 


or complete heart-block, resulting from myocardial lesions, 
is particularly prone to occur. Premature beats are com¬ 
mon. Less frequently, auricular fibrillation or other 
arrhythmia may obtain. 

There is nothing characteristic in the blood pressure 
readings in cardiovascular syphilis; it remains essentially 
normal unless aortic regurgitation or some condition (not 
syphilitic) causing hypertension complicates the case. 

As in other forms of syphilis, the Wassermann reaction 
has been found to vary from strongly positive to negative. 
There were 7, or 25 per cent., full negative results in 27 
Wassermann tests performed at the Massachusetts Gen¬ 
eral Hospital on cases proven shortly after, at autopsy, to 
have definite cardiovascular syphilis. 

Rontgen Findings. —It is inconsistent with our 
knowledge of the pathology of cardiovascular syphilis to 
expect that evidence of its presence can be obtained in 
early cases by radiographic examination. But in the more 
advanced cases, particularly when the aorta has undergone 
alteration in size and contour, the X-ray often produces 
very definite findings. 

A marked prominence of the aortic shadow to the right, 
just above that of the right auricle, is almost always due 
to syphilitic aortitis. A general enlargement of the 
shadow of the aorta may occur, but must be distinguished 
from the result of changes in the aortic curve, occurring in 
some other conditions. An aneurism, if present, is usually 
distinguished on radiographic examination. The value of 
this is better appreciated when it is remembered that in 
one half the cases of the saccular type, there are no sounds 
or murmurs over the aneurism. 


134 MODERN CONCEPTION OF HEART DISEASE 


If the width of the great vessels, obtained by Rontgen 
mensuration, is more than one half that of the heart, syphi¬ 
litic invasion of the aorta is almost certainly present. In 
doubtful cases, the mensuration should be repeated in a 
few weeks or months, to note if the aorta is increasing in 
size. The heart often shows enlargement more markedly 
in its long diameter, and especially in those cases in which 
insufficiency of the aortic valve is present. 

Diagnosis. —A clear distinction must be made between 
“syphilis of the heart” and “the heart in syphilis,” as it 
seems established that the heart is not involved in every 
patient suffering from syphilis. On the other hand, it 
is the part of wisdom to consider every patient known to 
have syphilis as a potential case of cardiovascular syphilis. 

Syphilis should be considered in any case of cardio¬ 
vascular degeneration of obscure origin. Every case of 
aortic insufficiency, or heart-block, developing in an adult 
not giving a clear history of rheumatic infection, should at 
once arouse the suspicion of specific disease. A definite 
history of syphilitic infection and a positive Wassermann 
reaction are of considerable value, but they may be absent. 
The observation of syphilitic skin lesions, or some other 
mark of lues, may suffice to turn a possible into a probable 
diagnosis of cardiovascular syphilis. The X-ray, in all 
but very early cases, usually gives the most definite con¬ 
firmatory findings. 

Though easy to diagnose in a typical and advanced case, 
cardiovascular syphilis is almost impossible to diagnose in 
the early or latent type. There is no one point on which a 
diagnosis is to be made, but each suspected case requires 
careful attention to the history, especially to the symptoms 


CARDIOVASCULAR SYPHILIS 


135 


and physical findings, and is to be checked up by radio- 
graphic examination and Wassermann test. It is only 
after all the facts have been collected that definite conclu¬ 
sions should be drawn, and at times only a tentative diag¬ 
nosis is possible. In this position the diagnosis may remain 
until the results of the therapeutic test for syphilis have 
been observed. This consists preferably of four to six 
injections of arsphenamine at weekly intervals, followed 
by a course of seven to eight intramuscular injections of a 
mercurial salt. Of less value, but for certain reasons 
sometimes employed, is the oral administration of hydrarg. 
cum creta 0.06 to 0.12 gm. (gr. i to ii) t.i.d ., with 0.3 to 1.2 
gm. (gr. 5 to 20) of potassium iodide t.i.d., for about 
six weeks. 

Differential Diagnosis. —N on-sypliilitic aortitis 
occurs 13 in rheumatic fever, influenza, septic heart disease, 
anthrax, erysipelas, small-pox, typhoid fever, diphtheria, 
measles, scarlet fever, pneumonia, malaria, tuberculosis, 
and gonorrhea. It is relatively rare, often symptomless, 
and usually overlooked. Even small aneurisms or per¬ 
forations may occur. Bennert 14 has established a rule that 
aneurism in children and in youths is a result of acute 
rheumatic fever. They are rare and happily have a 
marked tendency towards spontaneous recovery. It is 
perhaps enough to realize the existence of these non¬ 
syphilitic infections of the aorta, and in a case of aortitis, 
occurring after one of the above infections, the possibility 
of its non-syphilitic origin should be considered. 

Arteriosclerosis is often combined with syphilis in 

13 Reid, W. D.: Boston Med, and Surg. Jour., clxxxiii, No. 3:67, and 
4:105 (July 15 and 22, 1920). 

14 Bennebt, R.: Zeitsch. f. klin. Med., Bd. lxix, Nos. 1 and 2, 121. 



136 MODERN CONCEPTION OF HEART DISEASE 


elderly patients. Pure atheroma rarely causes insuffi¬ 
ciency of the aortic valve and practically never leads to 
the formation of an aneurism. Pain is present in but 
a small minority of the arteriosclerotic cases. The gross 
pathological findings differ, particularly in that there are 
fatty and calcareous changes as contrasted to the fibrosis 
of syphilis. The Rdntgen findings of the aorta show no 
bulging to the right of the ascending aorta, and less dilation 
of the arch, but rather a lengthening of the same with a 
prominence of the knob to the left. 

Hypertensive heart disease also causes enlargement of 
the heart and some dilation of the aorta, but may be dis¬ 
missed with the comment that neither high blood pressure 
nor evidence of impaired renal function form part of the 
picture of cardiovascular syphilis. 

Rheumatic heart disease at times must be considered. 
This is especially true if, in addition to the findings of 
aortic insufficiency, there is an apical murmur which may 
be explained, either as that described by Austin Flint, or as 
that of true stenosis of the mitral orifice. Organic change 
of the mitral valve is probably never syphilitic, and, if pres¬ 
ent, the insufficiency of the aortic valve may then also be of 
rheumatic origin. Evidence of enlargement of the left 
auricle and the electrocardiographic findings of mitral 
stenosis (which see) indicate the latter condition. True 
mitral stenosis, furthermore, tends to distinctly lessen the 
Corrigan quality of the pulse. The history is often of 
assistance; “apparently well until recently” and the absence 
of the story of an infection which might cause rheumatic 
heart disease, is not the history of a rheumatic heart. 
Nevertheless there are cases in which a distinct doubt must 


CARDIOVASCULAR SYPHILIS 


137 


remain. Resort to the therapeutic test of antisyphilitic 
treatment is then justified. 

Heart-block may likewise raise the question as to 
whether it be of rheumatic or luetic causation. The thera¬ 
peutic test is indicated in these cases also. 

Cases in a sanatorium for pulmonary tuberculosis have 
not infrequently first been correctly diagnosed cardio¬ 
vascular syphilis, as a result of radiographic examination. 

Mediastinal tumors may at times offer some difficulty 
in differentiation. A careful study, with a consideration 
of the data present, and especially the X-ray findings, 
will almost always enable the correct diagnosis to be made. 

Tabes dorsalis hardly needs differentiation save as 
regards the so-called cardiac crises in tabetic patients. As 
syphilitic infection of the heart and aorta is very common 
in the victims of tabes dorsalis, the practical importance of 
separating the cardiac crises in tabes from the anginal 
attacks of cardiovascular syphilis, if they be not one and 
the same condition, is much lessened. 

Prognosis. —On the whole the prognosis of syphilitic 
infection of the circulatory tissues is grave, because of the 
tendency to progressive impairment of the integrity of the 
heart and aorta. Angina pectoris, with its danger of sud¬ 
den death, may ensue. About 30 per cent, of the recog¬ 
nized cases (figures are of little value, as cardiovascular 
syphilis often escapes recognition) are estimated to develop 
aneurism or insufficiency of the aortic valve or both. A 
fatal hemorrhage from perforation of the aneurism is 
not unusual. 

On the other hand, evidence is now being accumulated 
that modern antisyphilitic therapy is being attended with 


138 MODERN CONCEPTION OF HEART DISEASE 


promising results. 15 The improvement is in symptoms and 
not in physical signs. Thus, diminution of the dilation 
of the arch of the aorta does not occur. Recollection of 
the pathology of cardiovascular syphilis makes it easy to 
comprehend why aneurism, aortic insufficiency, etc., cannot 
be removed. The average length of life in cases of a com¬ 
paratively advanced type, from the time treatment was 
instituted, 16 was one year where mercury and potassium 
iodide were employed, and three years when diarsenol, or 
its equivalent, was added. 

Considerable depends upon the amount of damage al¬ 
ready incurred before the diagnosis is established and treat¬ 
ment instituted. Thus, if insufficiency of the aortic valve 
has ensued, serious mischief has been achieved. Cardiac 
failure, especially if advanced to the stage of edema of the 
lower extremities, always offers a poor prognosis. 

Treatment. —This is primarily that of syphilis. Since 
it has been demonstrated that the spirochetes actually 
invade the heart and the aorta, the treatment should be 
directed toward destroying the invading organisms as 
quickly as possible. For this purpose arsphenamine, or 
its equivalent, and mercury are most useful. Syphilog- 
raphers, however, differ in the details of the administra¬ 
tion of these drugs. The relative merits of the methods 
advised by different authorities need not be entered into 
for the purposes of this book. A single method will be 
described which is suitable for the treatment of cardio¬ 
vascular syphilis and which, in addition, appears to be 
attended with a minimum of risk and has been observed to 
obtain favorable results. 

15 Reid, W. D.: Jour. Amer. Med. Assn., lxxiii: 1832, 1919. 

16 Ibid. 



CARDIOVASCULAR SYPHILIS 


139 


Arsphenamine, or a similar arsenical, should be injected 
intravenously in an initial dosage of about 0.15 gm., and, 
if well tolerated, rapidly increased to 0.5 gm. per dose. 
This latter amount should rarely be exceeded, as with this 
precaution, cardiac cases may be treated with but small 
risk of the occurrence of an unpleasant reaction. The 
course of arsphenamine should include six to ten injections 
at weekly intervals. At the same time the patient should 
receive mercury by mouth; suitable preparations are the 
protiodide of mercury gm. 0.01 to 0.015 (gr. V 6 to V 4 ), 
and mercury with chalk gm. 006 to 0.12 (gr. 1 to 2) t.i.d., 
p.c. On completion of the course of arsphenamine and mer¬ 
cury, treatment is continued by a series of fifteen intra¬ 
muscular injections of mercury given at one week intervals. 
For this the salicylate of mercury in a dosage of gm. 0.065 
to 0.13 (gr. 1 to 2) is a good selection. 

After the twenty to twenty-five weeks of treatment, 
outlined above, have been given, the patient is allowed an 
intermission of four to eight weeks, and then the course of 
arsphenamine and mercury is repeated. It is sometimes 
permissible to replace the mercurial injections by the oral 
administration or by inunctions of the drug. 

There may be times when, for certain reasons, it is not 
deemed possible to treat the patient by the above-mentioned 
courses of injections. In such cases mercury can at least 
be administered orally. Satisfactory preparations have 
been mentioned. As a rule it would seem that to-day 
mercury is rarely prescribed without the precaution of 
special care of the teeth, but in addition it should be empha¬ 
sized that attention be directed towards the diet. Mer¬ 
curial preparations often produce diarrhea of such severity 


140 MODERN CONCEPTION OF HEART DISEASE 


that the patient refuses to continue the use of the drug. 
This can usually be avoided by prescribing a diet which 
excludes the articles of food known to stimulate bowel 
action, i.e., fruits, green vegetables, coarse cereals, etc. 
The latter may be reintroduced if the drug is being 
well tolerated. 

Iodide of potassium is probably of use only in the cases 
coming under treatment years after the initial infection. 
It may be prescribed in doses of gm. 0.6 to 1.3 (gr. 10 to 
20) t.i.d.j p.c., for alternate two weeks over long periods. 
Some syphilographers prefer that the amount of the iodide 
should not exceed the smaller of the doses listed above. 

No patient should be dismissed as cured, but advice 
should be given that he report at six to twelve month inter¬ 
vals for re-examination and an opinion as to the need of 
further treatment. A return of active symptoms or evi¬ 
dence of a progression of the syphilitic lesions, regardless 
of the Wassermann reaction, should be an indication for the 
resumption of full treatment. 

Treatment may be further discussed according to the 
type of case. 

1. Cases in which the cardiac symptoms are present 
within a few weeks or months of the primary lesion of 
syphilis. The patient should be restricted to bed and 
antiluetic therapy instituted. There appears to be less 
danger of untoward results if mercury is administered first 
and followed within two or three weeks by a course of ars- 
phenamine. The patient may be allowed up after treat¬ 
ment has been carried out for two to three weeks and there 
is evidence of improvement. The further treatment is 
that described above. 


CARDIOVASCULAR SYPHILIS 


141 


2. Cases coming under treatment years after the pri¬ 
mary infection and exhibiting moderate physical signs with 
but little evidence of cardiac failure. The courses of 
arsphenamine, mercury, and potassium iodide, as already 
outlined, are indicated. Many feel that the maximum dose 
of arsphenamine should not exceed 0.3 or at the most 0.4 
gm. If angina pectoris is present, the measures suitable 
for that condition (see later chapter) should be added. 
The general hygienic measures recommended (see chapter 
on treatment) for the cardiopath should be prescribed. 

3. Cases with aneurism, heart-block, marked symptoms 
of heart failure, etc. If the heart failure is severe, treat¬ 
ment should first be directed towards its relief. The 
measures to be employed do not differ from those suitable 
for the treatment of heart failure of non-syphilitic origin. 
After some measure of control of the cardiac embarrass¬ 
ment has been obtained, treatment against the syphilitic 
infection should be instituted. It will usually be safer to 
commence with mercury. After two to three weeks it may 
be proper to administer arsphenamine, starting as low as 
gm. 0.05 to 0.1 and not exceeding perhaps gm. 0.3 Mer¬ 
cury, in the form of pills or as an inunction, and iodide of 
potassium have the same indications as described above. 

Discussion of the special treatment of aneurisms will 
be postponed to a subsequent chapter. 


CHAPTER X 

ARTERIOSCLEROTIC HEART DISEASE 

Arteriosclerotic heart disease is sometimes termed 
the senile heart. When considered in this sense, it can 
hardly be termed a disease, but may better be considered 
a process of involution. Since symptoms may occur and 
since a fair proportion of the cases occur a little before the 
onset of old age, it seems better for clinical purposes that 
arteriosclerotic changes should continue to be regarded as 
one type of heart disease. 

It has long been the custom to include cases with high 
blood pressure, namely, cases with some form of hyper¬ 
tensive heart disease, under the term of arteriosclerosis, but, 
as so strongly urged by Allbutt, it no longer seems intelli¬ 
gent to do so. 

Etiology. —Apparently there are so many factors 
involved in the production of arteriosclerosis that it is 
hardly possible to speak with assurance of any one. When 
the condition is not evident until old age, it is customary 
to state that the arteriosclerotic changes are due to the 
advanced years and the wear and tear of life. 

In recent years, evidence, some of which is confirmed 
by experimental work, has accumulated that pneumonia, 
typhoid fever, the exanthemata, and, in fact, most of the 
infectious diseases, are followed by some degree of arterio¬ 
sclerotic changes. Excessive mental strain 1 would appear 
to be a potent factor. The absorption of lead is held by 
some to produce sclerotic changes. 

1 Muller, Friedrich: Arch. Int. Med., 1 : 1, 1908. 

142 



ARTERIOSCLEROTIC HEART DISEASE 


143 


Pathology. —In the early stages the intima shows 
yellowish placques or streaks which take the stain for fat. 
Then bluish-white, translucent connective tissue forms 
round the placque. MacCallum * 2 describes these as having 
the appearance of drops of paraffin on the intima. The 
internal elastic lamella under the placques is often frayed 
and the smooth musculo-elastic layer of the intima may 
be destroyed. The centre of the placque is soft, and, if the 
roof breaks through, the contents are washed away in the 
blood stream, with the resulting production of an atherom¬ 
atous ulcer. Thrombus formation is then likely. De¬ 
posits of cholesterin and the phosphates of calcium and 
magnesium are found in the process. 

In the main the media is not much involved save in the 
smaller arteries, where some thinning and fat deposit are 
found. The type of sclerosis described by Monckeberg, 2 
which may be a different process from true arteriosclerosis, 
occurs mostly in the arteries of the leg. In this form of 
sclerosis masses containing fat, lime, and even bone with 
marrow, are found in the media. The intima does not 
always show thickenings over it, though the type of intimal 
sclerosis described above may occur along with Moncke¬ 
berg’s sclerosis. 

The aorta is usually dilated and lengthened so that it 
curves from one side to the other of the vertebral column. 
In the branches, the placques may distinctly diminish the 
calibre of the vessel by encroaching upon the lumen. At 
times large masses are present which practically oblit¬ 
erate the lumen of the arteries and produce gangrene. 

2 MacCallum, W. G. : Text-book of Pathology, W. B. Saunders Co., Phila¬ 
delphia, 1916, p. 322. 

2 Ibid. 



144 MODERN CONCEPTION OF HEART DISEASE 


MacCallum states that these may or may not be organ¬ 
ized thrombi. 

The heart tends to be small, and the myocardium thin¬ 
ner than usual. The heart muscle is often of a brownish 
hue, the so-called “brown atrophy,” and feels flabby to 
the fingers. On histological examination the brown atro¬ 
phy may be recognized by the brown pigment granules. 
Fragmentation of the muscle fibres is common. In some 
cases, in which hypertension is associated with arterio¬ 
sclerotic heart disease, the pathology shows a mixed picture; 
i.e.j there is some hypertrophy of the muscle fibres and 
areas of replacement by fibrosis. 

The heart valves, especially the aortic and mitral, may 
become thickened and puckered. Deposits of lime in these 
valve thickenings are common. 

Symptoms and Signs. —Varying degrees of a lowering 
of the power of the heart may be observed. In the average 
case, the diminution of the cardiac strength comes on gradu¬ 
ally and is only a part of the general decline of the physical 
powers that occurs in normal old age. Elderly persons 
show a distinct tendency to lessen their physical activities, 
and it may be only as a result of some sudden or unusual 
exertion that attention is drawn to the heart. Occasionally 
the picture of angina pectoris may be present. 

Arteriosclerotic heart disease is commonly but part of 
general arteriosclerosis; certain symptoms, not primarily 
cardiac in origin, are therefore often present in these 
patients. A change in the mental faculties, varying from 
a lessening of the power of memory to the condition of 
senile dementia, may be observed. A tendency to headache 
infrequent. The latter has been explained on a circulatory 


ARTERIOSCLEROTIC HEART DISEASE 


145 


basis, as due to a congestion in the cerebral circulation. 3 
Dizziness, on change from the horizontal to the upright 
position, or on stooping, is due to a sluggishness of the 
vasomotor reflex, by which, in the normal individual, a 
physiological adjustment is promptly made for the main¬ 
tenance of a normal circulation in varying postures of the 
body. Discomfort or pain in the calf of the leg on walking 
appears to be due to the failure of the increase in blood 
supply needed in the leg muscles during exercise. Other 
symptoms of general arteriosclerosis need not be men¬ 
tioned here. 

On physical examination the peripheral arteries show 
changes to palpation. The wall feels thickened and more 
rigid, and in cases where deposition of lime salts has 
occurred, the artery may give a beaded sensation to the 
palpating Anger. A marked degree of the latter condition 
is sometimes termed the “pipe-stem artery.” The blood 
pressure is usually not essentially changed, ranging from 
a little below to a little above the normal adult level. It 
is a mistake to hold that any degree of increased blood 
pressure is the rule in arteriosclerosis, as in by far the 
majority of such patients the blood pressure readings are 
within normal limits. 

An increase of the supracardiac dulness, as well as a 
visible or palpable pulsation in the suprasternal notch, 
may often be noted. They are produced, of course, by the 
elongation and consequent change in the position of the 
aorta, which occurs in arteriosclerosis. 

The Rontgen examination typically discloses a heart 

3 Inman, T. G.: “ Cerebral Thrombosis and Abrupt Slowing of the Cerebral 
Circulation,” Jour. Amer. Med. Assn., 75, 26: 1765 (Dec. 25, 1920). 

10 



146 MODERN CONCEPTION OF HEART DISEASE 


slightly smaller than normal and a prominence of the aortic 
knob to the left. 

By the usual clinical methods of examination, the heart 
appears to be of normal size or sometimes a little small. 
The frequent concomitance of emphysema of the lungs 
may obscure the borders of the cardiac dulness. The 
sounds are likely to be somewhat less loud than in younger 
individuals. The second aortic sound is commonly of a 
duller quality, perhaps due to a thickening of the semilunar 
cusps and adjacent tissues. A systolic murmur, generally 
soft in quality, often accompanies the apical first sound, 
and a louder, rougher murmur, transmitted outward and 
to the neck, may be associated with the first sound at the 
second right costal cartilage. The diastolic murmur of 
an insufficiency of the aortic valve is relatively rare. 

Extrasystoles, or premature beats, are common in the 
arteriosclerotic heart. Less commonly, fibrillation of the 
auricles will be found to be the cause of an irregularity of 
the cardiac rhythm. Heart-block is a still further 
complication. The latter two are often present at the 
same time. 

Diagnosis. —The appearance of symptoms of an insuf¬ 
ficient circulation in an elderly patient, or in one in whom 
the general or peripheral signs of arteriosclerosis are pres¬ 
ent, should immediatelv draw attention to the heart. The 
dull quality of the second sound at the aortic area is helpful 
but not diagnostic, as a similar change may be found in 
cardiovascular syphilis. The murmurs should not mislead 
one, as they are merely part of the picture of the arterio¬ 
sclerotic heart, and do not indicate an infection such as that 
occurring in rheumatic heart disease. It should be remem- 


ARTERIOSCLEROTIC HEART DISEASE 147 

bered that certain of the arrhythmias, i.e., premature beats, 
auricular fibrillation, and heart-block, are common in arte¬ 
riosclerotic disease. Angina pectoris, appearing in a 
patient over fifty-five years of age, points to arteriosclerotic 
changes in the heart, as a rule. If the blood pressure is 
persistently elevated, the condition is probably not true 
arteriosclerotic heart disease, but some form of hyper¬ 
tensive heart disease. 

Prognosis. —It is not to be expected that arterioscle¬ 
rotic changes in the circulation should disappear. A slow 
progression is the rule. Those cases which make their 
appearance before true old age, as, for example, those 
which appear to be the result of infections or severe ner¬ 
vous strain, tend to advance to a considerable degree of 
circulatory impairment. The general deterioration of the 
patient can be considerably checked by judicious treatment. 

Treatment. —The first essential is an intelligent regu¬ 
lation of the patient’s life. All chafing at the lessening 
of the physical and mental powers is to be discouraged 
and combated by tactful explanation of the futility of the 
same, and conversation directed towards a philosophical 
acceptance of the situation. Experience has shown that 
elderly people are benefited by association with young 
people. It tends to keep them more cheerful and inter¬ 
ested in life. 

Daily exercise of a light character will do much to 
maintain the general health. Walking and light golf are 
examples of suitable exertion. 

An extra amount of rest is indicated. There is reason 
to believe that such patients do better and have less head- 


148 MODERN CONCEPTION OF HEART DISEASE 


ache from cerebral congestion 4 if the sleeping periods are 
not too long, and therefore the patient should not be 
encouraged to remain in bed late in the morning. One 
or more periods during the day may be arranged for a nap. 

Diet .—Since the teeth are usually absent or deficient, 
the food should be such that does not require much chewing. 
In consideration of the fact that there is less hydrochloric 
acid in the gastric juice, and digestion is slower, the food 
should be simpler, moderate in amount, and the meals 
preferably not less than four hours apart. In certain 
respects the diet should revert towards that suitable in 
early life. 

Drug treatment is of secondary importance. At times 
drugs may be used to relieve symptoms. Strychnine, qui¬ 
nine, arsenic, etc., are often prescribed as tonics. Various 
bitters, as stomachics, and laxative medicines are often 
used. In deciding whether to give a medicine, it seems 
wise not to overlook the favorable psychic effect when 
dealing with a patient who believes strongly in drugs. 

Digitalis .—It is doubtful if this drug is of any benefit 
to the arteriosclerotic heart, if normal rhythm is present. 
If given, it should be prescribed tentatively and in small 
dosage. Decision as to the continuance of the drug may 
be based on the effect observed. 

* Inman, T. G.: “ Cerebral Thrombosis and Abrupt Slowing of the Cerebral 
Circulation,” Jour. Amer. Med. Assn., 75, 26: 1765 (Dec. 25, 1920). 



CHAPTER XI 

HYPERTENSIVE HEART DISEASE 

This title applies to a group of conditions in which 
the essential feature is a persistent elevation of the blood 
pressure. There are three types which are often suffi¬ 
ciently distinct to permit recognition. The first, for which 
the term “chronic vascular hypertension” seems satisfac¬ 
tory, has been described in the literature under other names, 
i.e.. Allbutt’s hyperpiesis, essential or primary hyperten¬ 
sion, chronic hypertensive cardiovascular disease, arterio¬ 
sclerosis, etc. The second type, “chronic hypertension 
with diabetes,” usually of mild degree, differs little save in 
the disturbance of the sugar metabolism. The third form 
is satisfactorily labelled, it would appear, “chronic hyper¬ 
tension with nephritis.” Although these three types may 
usually be distinguished by careful study, and it has been 
urged that at least the first and third form obtain separate 
classification, it would appear consistent with the cardiac 
aspects, and more in accordance with the present state of 
our knowledge, to resist the temptation to break up 
the group. 

Etiology. —The age of the patient varies from as low 
as twenty-five years to old age, with a marked predomi¬ 
nance of the decades forty to fifty and fifty to sixty. The 
causation of hypertensive heart disease is as yet obscure. 
Overeating and mental strain or worry appear to be pro¬ 
vocative agents. Disturbances of the ductless glands, 
particularly the condition of hyperthyroidism, is often 
associated. The importance of a change in the function 

149 


150 MODERN CONCEPTION OF HEART DISEASE 


of the ovaries has been emphasized by Hopkins , 1 who 
believes that there is a distinct type of hypertension occur¬ 
ring at the menoj)ause. That this latter should be sepa¬ 
rated from the larger group is uncertain. The role of 
certain poisons and infections is not yet clear. The devel¬ 
opment of the studies in the chemistry of the blood has 
brought to light that the salt metabolism is nearly always 
disturbed. The threshold for the excretion of salt is high . 2 
Judgment as to the etiological importance of certain factors 
is often hampered by the fact that many cases are not noted 
until the patient has reached the age at which appear the 
arteriosclerotic changes associated with the onset of old age. 
In fact, it is only of recent years that an attempt has been 
made to separate chronic vascular hypertension from invo¬ 
lutionary arteriosclerosis. 

Pathology. —In the early or presclerotic cases, au¬ 
topsy may fail to disclose arterial or renal disease. The 
hypertension appears to be functional, due to a hypertonus 
of the arterial musculature, thereby producing a narrow¬ 
ing of the lumina of the arterioles in the precapillary area. 
In the majority of cases, within a few months, to one or 
two years, there ensue sclerotic changes in the arterial walls 
and hypertrophy of the myocardium. The arterial changes 
do not differ essentially from those found in arteriosclerosis 
without hypertension. The kidneys commonly show mod¬ 
erate change of the character occurring in arteriosclerosis. 
The renal changes may be somewhat more marked in the 
cases diagnosed clinically hypertension with nephritis. 

1 Hopkins, A. H.: “Climacteric Hypertension,” Amer. Jour. Med. Sci., 6, 
clvii: 826, 1919. 

2 Allen, F. M.: “Arterial Hypertension,” Jour. Amer. Med. Assn., 74, 
10:652 (March 6, 1920). 



HYPERTENSIVE HEART DISEASE 


151 


The cardiac change, however, as so well emphasized by 
Allbutt , 3 is radically different from that obtaining in 
arteriosclerosis. The myocardium is hypertrophied rather 
than degenerated. It is thicker and on microscopic exam¬ 
ination its fibres are increased in number and size. At a 
later stage, when cardiac insufficiency appears, the heart 
muscle shows necrosis of some of the muscle fibres, with 
replacement by fibrous tissue, a form of fibrous myocarditis. 
The aortic and mitral valves are not infrequently thickened 
and puckered. In cases coming to section, after death 
caused by cerebral hemorrhage, the presence of the latter 
will, of course, be added to the post-mortem findings. 

Symptoms. —Many of these cases are first found in 
the course of a routine physical examination which has been 
prompted because of some intercurrent disease. The indi¬ 
vidual often appears robust but in a state of overtension. 
The type has been pictured thus: “The patients are over¬ 
weight and sometimes even obese. The neck is short, the 
muscles are soft, their bodily movements are sluggish, their 
carriage and walk are ungraceful, and they lack the spring 
and elan of the former athlete. Physically these people 
are tense; they pursue their vocation with tremendous 
seriousness and worry over trivialities. Phlegm and 
hypertension are, in my experience, antagonistic. Fur¬ 
thermore, these patients have narrow intellectual horizons. 
Their interest in anything outside of their business is desul¬ 
tory. They have no hobbies .” 4 

Gastric symptoms may lead the patient to consult a 

3 Allbutt, C. A.: Diseases of the Arteries, Including Angina Pectoris, 

1915, Macmillan & Co., Ltd. 

4 Moschcowitz, E.: “ Hypertension: Its Significance, Relation to Arterio¬ 
sclerosis and Nephritis, and Etiology,” Amer. Jour. Med. Sci., 158:668 
(Nov., 1919). 



152 MODERN CONCEPTION OF HEART DISEASE 


physician. These complaints are of the type consistent 
with gastric neurosis; gas formation and constipation may 
be prominent. In other individuals nervous symptoms 
and pains in the legs are conspicuous. Headache is com¬ 
mon. A little shortness of breath and evidence of cardiac 
failure may make their appearance. In more advanced 
or complicated cases, the signs and symptoms of marked 
heart failure, angina pectoris, or cerebral hemorrhage may 
be present. Weakness, vertigo, and epistaxis are still 
further symptoms. Patients in whom hypertensive heart 
disease is associated with nephritis appear sicker and often 
have an anemia in addition. Edema is a more frequent 
condition in this type of hypertensive heart disease. 

Physical Signs. —The sphygmomanometer shows a 
constant elevation of the systolic and diastolic blood pres¬ 
sures ; the former may be as high as 300 or more, while the 
latter may even reach 190. While it is known that the 
blood pressure varies in accordance with age, sex, and 
other factors, it seems a reasonable rule to consider hyper¬ 
tension present if the systolic pressure exceeds 150 or 160 in 
men, and 140 or 150 in women, and the diastolic above 
100 in either. 

Examination of the heart may give normal findings, 
but if hypertrophy has ensued the apex impulse is usually 
displaced downward and to the left, and, other things 
being equal (i.e., the contact of the heart with the chest 
wall, the thickness of the parietes, etc.), is more forcible in 
character. The area of deep cardiac dulness is increased 
in accordance with the extent of the left ventricular en¬ 
largement. The width of the supracardiac dulness com¬ 
monly shows an increase due to the broadening of the 


HYPERTENSIVE HEART DISEASE 


153 


arch of the aorta. On auscultation the first sound at the 
apex is usually of a more booming character and the second 
sound at the level of the second right costal cartilage is 
accentuated. There are no murmurs characteristic of 
hypertensive heart disease. A systolic murmur at the apex 
may indicate an insufficiency of the mitral valve, of muscu¬ 
lar causation, and a systolic murmur at the aortic area 
may result from the relative dilatation of the first part of 
the aorta. The rhythm is normal, but it may be interrupted 
by an abnormal rhythm, especially by premature beats, 
as in other types of heart disease. 

Ophthalmoscopic examination may show sclerosis of 
the retinal arteries and occasionally hemorrhage in addition. 

Urinary examination generally discloses the presence 
of albumin varying in amount from a very slight to a large 
trace, with a few to many hyalin and granular casts. The 
tests of the functional power of the kidneys demonstrate a 
difference between the types of hypertensive heart disease. 
In the first two, i.e., chronic vascular hypertension and 
hypertension with diabetes, there is commonly no reduction 
in renal function save in the handling of sodium chloride. 5 
The chloride content of the blood plasma and the renal 
threshold of salt excretion are both high. In the cases of 
hypertension with nephritis, these tests will disclose, in 
addition, some fixation of the specific gravity of the urine, 
a diminution in the ability to excrete phenolsulphoneph- 
thalein, and an increase in the blood urea content, etc. 
When diabetes is associated with hypertensive heart dis¬ 
ease, sugar may be detected in the urine, or the blood 
chemistry may show abnormalities in relation to sugar. 

'Allen, F. M.: “Arterial Hypertension,” Jour. Arner. Med. Assn., 74, 
10:652 (March 6, 1920). 



154 MODERN CONCEPTION OF HEART DISEASE 


Rontgen examination may give normal cardiac outlines, 
or, if hypertrophy has occurred, the heart shadow is in¬ 
creased in its long diameter and in the region of the left 
ventricle. The width of the great vessels shows mod¬ 
erate increase. 

The electrocardiogram in a typical case shows left pre¬ 
ponderance, often of marked degree. 

Diagnosis. —The earliest and essential point is the 
elevation of the hlood pressure. The decision that true 
hypertension is present should be based on the finding of 
high pressures on examination with the sphygmomanom¬ 
eter at several different occasions, and after due allowance 
has been made for temporary elevation caused by transient 
emotional factors. Judgment should likewise be withheld 
as to the presence of hypertensive heart disease if the 
patient is suffering from some febrile disease, such as pneu¬ 
monia, which may depress the blood pressure below its 
normal level. Evidence of hypertrophy of the left ventri¬ 
cle is of distinct confirmatory value. 

A test for the rate of the metabolism is frequently of 
value. If the patient is at the time of the menopause, a 
disturbance of the balance of the ductless glands is to 
be considered. 

Studies of the renal function and of the blood chem¬ 
istry are necessary in order to differentiate the individual 
types of hypertensive disease of the heart. The fact that 
cases occur in which the findings are intermediate between 
the three forms of hypertension serves to emphasize that 
an absolute separation would be purely arbitrary. 

In the late stages, with marked evidence of cardiac 
failure, the effect of treatment will do much to differentiate 


HYPERTENSIVE HEART DISEASE 


155 


whether the heart or the kidney is the primary cause. If 
the heart responds well to digitalization, the case is cardiac 
rather than nephritic. If edema is present, three doses of 
theobromin sodium salicylate (diuretin) 1 gm. (gr. xv), 
or theophyllin sodioacetate (theocin) 0.3 gm. (gr. v) every 
four hours for four to six doses, may be given. If 
the kidney responds well the underlying condition is 
not nephritic. 

Arteriosclerosis is readily excluded by its essentially 
normal blood pressure. Cardiac hypertrophy is not a fea¬ 
ture of arteriosclerosis. The latter may, however, be pres¬ 
ent in addition to the hypertensive heart disease. 

Prognosis. —Since the nature of hypertension is not 
yet clearly understood it follows that the prognosis in indi¬ 
vidual cases cannot be depicted with certainty. Experi¬ 
ence, however, has demonstrated that the prognosis varies 
according to the type of hypertensive heart disease. 

In chronic vascular hypertension, judicious treatment, 
if undertaken early, may arrest or materially check the 
process so that the patient may live in comparative comfort 
for many years. If the patient is much overweight, 
accustomed to overindulgence in food, or subject to exces¬ 
sive nervous strain, there is greater prospect of benefit 
from treatment than there is in patients exhibiting less 
evident points of attack. When the condition does not 
yield to treatment there is always danger of sudden death 
from cerebral hemorrhage or less frequently from angina 
pectoris. A more gradual death from cardiac insufficiency 
terminates probably the majority of cases, and in the 
experience of the writer, this form of heart complication 
is more frequent than is angina pectoris. A few cases 


156 MODERN CONCEPTION OF HEART DISEASE 


progress to marked impairment of the kidneys and suc¬ 
cumb to uremia. 

Hypertensive heart disease with diabetes often does 
well on the dietetic treatment of diabetes or obesity. In 
the main, its prognosis appears similar to that of chronic 
vascular hypertension. 

The third type, namely, hypertensive heart disease with 
nephritis, has the least favorable prognosis. A return to 
normal health is unusual; some degree of anemia and weak¬ 
ness usually persist. Within a few years the majority of 
such patients succumb to progressive impairment of the 
kidney, and uremia. 

Treatment must be based upon an accurate diagnosis, 
with a recognition if possible of the type of hypertensive 
disease. Granting that it may not be possible to state 
just what caused the heightened blood pressure in an indi¬ 
vidual case, it seems reasonable to lessen those factors 
which the study of physiology has shown cause a rise in 
the blood pressure level. 

The early and less advanced cases should be treated 
by modification of their life so as to reduce the intake of 
food and the outgo of nervous energy. In the diabetic 
type the diet suitable for a case of mild diabetes is usually 
beneficial. If evidence of kidney impairment predomi¬ 
nates, the dietetic measures suitable for nephritis should be 
followed. In all cases the amount of food should be low. 

The salt intake is of special importance. In many 
cases it is enough to reduce the amount of salt, but if the 
hypertension persists it may be necessary to carefully 
arrange a diet in which the salt does not exceed 2 gm. 


HYPERTENSIVE HEART DISEASE 157 

(30 gr.) per day.' 1 In the nephritic type, however, it may 
sometimes be necessary to give more than 2 gm. (30 gr.) 
for its diuretic effect and the prevention of uremia. In 
the cases, then, which do not yield to simpler measures, it 
is doubly indicated to obtain the help of chemical analysis 
of the blood and to guide the treatment largely by its 
findings. Further discussion of this is beyond the scope 
of this book; it is more the treatment of nephritis than that 
of cardiac disease. 

The amount of fluid intake should usually be reduced. 
It is true that some patients do well on two to three litres 
per day, but many are benefited by keeping the amount 
down to one or one and a half litres, or less. A recent 
report, * * 7 however, announces very favorable results from 
the addition of water to the daily intake. 

Constipation, if present, should be relieved, preferably 
by the non-drug methods, i.e., regular time for going to 
stool, diet, suds enemata, liquid petrolatum U.S.P., etc. 
Although it is not good practice from the standpoint of the 
treatment of the constipation problem, there is much clin¬ 
ical evidence that patients suffering from chronic vascular 
hypertension are benefited by an occasional dose of salts, 
castor oil, or calomel. 

The condition of tension and mental strain should he 
met by ascertaining its cause and removing the latter if 
possible. Herein lies an opportunity for the physician to 
use all his tact and diplomacy in correcting by judicious 
conversation the patient’s philosophy of life, which is nearly 

8 Allen, F. M.: “Arterial Hypertension,” Jour. Amer. Med. Assn., 74, 

10:652 (March 6, 1920). 

7 Orb, J. B., and Innes, I.: “The Effect on Arterial Hypertension of 
Increased Fluid Intake,” Brit. J. Erper. Path., 3:61, 1922. 



158 MODERN CONCEPTION OF HEART DISEASE 


always faulty. The patient exhibiting hypertensive heart 
disease will be found in the majority of cases to be at odds 
with his environment. It is often helpful if the patient 
can be induced to read one or more of the little books writ¬ 
ten by Dr. George Lincoln Walton . 8 Much good may 
result if the play element can be introduced into 
the patient’s life. A vacation is often indicated. The 
amount of work done by the patient may well be 
reduced by persuading him or her to turn over many of 
the minor items to subordinates. Some form of light out¬ 
door exercise is generally beneficial. Golf and walking 
are examples. 

A warm cleansing bath every other night, with a warm 
salt bath, of seven to ten minutes’ duration, on the alternate 
nights, produces a general vascular relaxation and pro¬ 
motes sleep. Temporary use of the milder sedatives and 
hypnotics may be resorted to in cases manifesting excessive 
nervous tension. 

If the rate of metabolism is high, treatment suitable for 
hyperthyroidism should be added. In cases occurring in 
women at the time of the menopause, a trial may be made 
of corpus luteum, or extract of the whole ovarian gland. 

In the more severe or advanced cases, rest in bed for 
two to three weeks, or, less safely, sweat baths may be tried. 
Symptoms are to be met. Venesection, with the removal 
of 350 to 500 or more c.c. of blood, appears to benefit 
intractable cases. Such a procedure repeated at intervals 
of three to twelve months has been followed bv considerable 
relief in selected cases. Nevertheless, it should not be 

8 “ Why Worry,” J. B. Lippincott Company, 1908. 

“Those Nerves,” J. B. Lippincott Company, 1909. 

“Calm Yourself,” Houghton, Mifflin & Co., 1913. 



HYPERTENSIVE HEART DISEASE 


159 


resorted to indiscriminately, and should in no wise cause 
a relaxation in the therapeutic measures already mentioned. 

While drug treatment is less satisfactory for cases of 
hypertensive heart disease, it seems at times to be indicated, 
particularly for the relief of symptoms. The nitrites, 
especially nitroglycerine, are employed, and more recently 
benzyl benzoate. (For further details on these drugs and 
the therapy of angina pectoris, the reader is referred to 
the chapter on the latter condition.) 

Severe cardiac failure, edema, or the various arrhyth¬ 
mias are to be treated essentially the same as when present 
in heart disease of other causation. 


CHAPTER XII 

THE HEART IN HYPERTHYROIDISM 

The heart in hyperthyroidism exhibits signs and causes 
symptoms sufficiently distinctive to warrant its description 
as a cardiac entity. It may be said that symptoms refer¬ 
able to the heart are present at some time in practically 
every case of hyperthyroidism. 

Etiology. —It is generally held that the condition is 
due to the action of the secretions of the abnormal thyroid 
gland directly on the myocardium or on the nerves control¬ 
ling the heart. A suspicion exists, however, that secondary 
infections may play an important part. It has been noted 
in the laboratory, that animals suffering from hyperthy¬ 
roidism, produced experimentally, are especially prone to 
incur various infections. This fact naturally suggests the 
possibility that many of the cardiac changes in man may be 
the result of infections. 

Pathology.— This is not well understood, perhaps be¬ 
cause too few hearts of patients suffering from hyper¬ 
thyroidism have been subjected to careful histological 
study. Goodpasture 1 reports two cases in which myo¬ 
cardial necrosis was demonstrated. The process was very 
extensive and diffuse in one, and limited and focal in the 
other. He ascribes the necrosis of the muscle cells as due 
to a toxic myocarditis and not to occluding vascular lesions 
or local infection. A similar condition, though rare in 
adults, occurs in children in association with extreme intoxi¬ 
cation, usually by diphtheria or scarlet fever. Good- 

1 Goodpasture, E. W.: Jour. Amer. Med. Assn., 76, 23:1545, 1921. 

160 



THE HEART IN HYPERTHYROIDISM 


161 


pasture, however, believes it is better perhaps to regard 
the necrosis as a result of an injurious agency other than 
that responsible for the underlying cardiac disease. 

The gross post-mortem appearances of the heart in 
hyperthyroidism are dilatation of the right chambers, mod¬ 
erate hypertrophy of the left ventricle, and slight fatty 
change. Goodpasture, 1 again, is authority for the state¬ 
ment that there are few instances on record in which actual 
destructive lesions of heart muscle have been observed in 
exophthalmic goitre, even in those dying of cardiac failure. 

Symptoms and Physical Signs. —In early cases, a 
tachycardia is present, but is unaccompanied by signs of 
myocardial change. With persisting rapid heart action, 
enlargement may become evident. An increased pulsation 
over the right ventricle is usually to be observed. Pro¬ 
gressive enlargement and overaction is followed by damage 
to the myocardium, which may be manifested by the ap¬ 
pearance of an arrhythmia, such as auricular fibrillation, 
auricular flutter, heart-block, etc. Sinus arrhythmia and 
premature beats may also be in evidence. Hypertension 
occurs in some cases of hyperthyroidism. 

The tachycardia of hyperthyroidism persists day and 
night. It is usually between 90 and 120, and is subject 
to considerable variation in rate following exercise, excite¬ 
ment, rest, etc. 

It is not to be supposed that the heart in hyperthyroid¬ 
ism can be satisfactorily understood unless the observer is 
familiar with hyperthyroidism as it affects the patient as 
a whole. In the absence of laboratory support the cardiac 
symptoms should rarely be ascribed to hyperthyroidism 

‘Goodpasture, E. W.: Jour. Amer. Med. Assn., 76, 23:1545, 1921. 

11 



162 MODERN CONCEPTION OF HEART DISEASE 


save in the presence of several of the main symptoms, 
such as: tremor, thyroid enlargement, exophthalmos, 
retraction of the upper eyelid, loss of weight, increased 
appetite, pronounced motor restlessness, emotional insta¬ 
bility, or sensations of heat, undue sweating, diarrhea, 
polyuria, etc. 

Hypersensitiveness to epinephrin may be noted in many 
patients, but not in all with hyperthyroidism, and it also 
occurs in others in whom this disease may be excluded. 
The clinical significance of the reaction is not clear, but at 
present it should certainly not be regarded as having any 
specific significance in the diagnosis of hyperthyroidism . 2 

The determination of the basal metabolism, where facil¬ 
ities therefor are available, offers very valuable assistance 
in the diagnosis of hyperthyroidism. Save for a moderate 
elevation in fever of the rate of the basal metabolism, the 
finding of an increased rate indicates hyperthyroidism. 
In the main there may be said to be two types of hyper¬ 
thyroidism ; in one, the sympathetic type, the pulse rate is 
elevated to a greater degree than the rate of the metabolism, 
and in the other, the vagotonic type, the reverse holds true. 
The prognosis is better, according to Means , 3 in the sym¬ 
pathetic type. 

The electrocardiographic findings have been discussed 
by Krumbhaar , 4 and White and Aub . 5 There are no data 
of pathognomonic significance. The T wave is usually 
of increased amplitude, but apparently there is a very 
limited parallelism between the height of this wave and the 

2 Peabody, F. W., Sturgis, C. C., Thompkins, E. M., and Wearn, J. T. : 
Amer. Jour. Med. Sci., 161, 4:508 (April, 1921). 

3 Means, James H.: Med. Clin. No. Amer., 3, 4:1092 (Jan., 1920). 

4 Krumbhaar, E, B.: Amer. Jour. Med. Sci., 1918, 155, 175. 

B White, P. D., and Aub, J. C.: Arch. Int. Med., 1918, 22, 766. 



THE HEART IN HYPERTHYROIDISM 


163 


basal metabolism. The electrocardiogram has, of course, 
its usual value in the accurate diagnosis of and the perma¬ 
nently recording of the various arrhythmias that may affect 
the heart. 

In patients in whom the hyperthyroidism has ceased 
spontaneously or following treatment, the heart may show 
evidence of permanent damage. Thus, auricular fibrilla¬ 
tion or some other functional disturbance may be present. 
In such cases, the signs and symptoms of cardiac impair¬ 
ment may not differ from those present in disturbances of 
other causation, and their connection with a previous 
hyperthyroidism may be appreciated only by the history 
of the occurrence of the latter condition. 

Diagnosis. —According to Friedrich Muller , 6 about 
one third of the cases affected by moderate palpitation are 
of thyroid origin. The diagnosis depends upon some of 
the above-mentioned signs and symptoms of abnormality 
of the heart, in association with evidence of hyperthyroid¬ 
ism. An unstable tachycardia is strongly suggestive of 
hyperthyroidism. Electrocardiographic evidence may be 
helpful. An elevation of the rate of the basal metabolism 
proves the diagnosis. 

Paroxysmal tachycardia differs in that it is usually of 
limited duration, of sudden onset and ending, and the heart 
rate in an individual attack varies not more than a few 
beats for change of posture, exercise, etc. Vagal pressure 
and the manoeuvres which abolish some attacks of paroxys¬ 
mal tachycardia will not so affect the tachycardia of 
hyperthyroidism. 

The tachycardia of effort syndrome, cardiac neurosis, 

8 Muixer j Friedrich: Arch. Int. Med., 1:1 (March, 1908). 




164 MODERN CONCEPTION OF HEART DISEASE 


etc., does not last day and night and gives more evidence 
of being of reflex origin. 

After the hyperthyroidism has ceased, the history of 
that disease may be necessary to explain the cause of 
cardiac impairment. 

Prognosis. —If the existing intoxication is the chief 
factor in the production of the arrhythmia, the latter may 
disappear with successful treatment of the hyperthyroid¬ 
ism. As previously noted, the prognosis is somewhat better 
in cases in which the pulse rate is elevated out of proportion 
to the increase in the rate of metabolism, i.e., in the so-called 
sympathetic type. Damage of the myocardium, evident 
after the cessation of the hyperthyroidism, is permanent. 

Treatment. —This is essentially that of the underly¬ 
ing condition, the hyperthyroidism. The chief measures are 
rest, Rontgen radiation of both thyroid and thymus glands, 
and surgical measures. When auricular fibrillation is 
present digitalization is indicated before surgical treat¬ 
ment is undertaken. 

There is experimental evidence 7 that chloroform as an 
anesthetic in hyperthyroidism is apt to be exceptionally 
detrimental to the myocardium, and should be avoided. 

T Goodpastube, E. W.: Jour. Exper. Med., Baltimore, 34, 4:407 (Oct. 
1, 1921). 



CHAPTER XIII 
THE HEART IN DIPHTHERIA 

It is well known that the heart is frequently, and some¬ 
times seriously, affected in diphtheria. The changes are 
sufficiently unique to warrant description. 

Etiology. —This is primarily, of course, that of diph¬ 
theria, namely the Klebs-Loffler bacillus. But pathology 
teaches that the organisms remain at the site of membrane 
formation, and that the internal damage is the result of 
absorption of the toxin secreted by the diphtheria bacilli. 
It might reasonably be thought that some of the heart 
damage is due to the invasion of secondary organisms, in 
a similar manner as the streptococci, staphylococci, etc., 
are known to cause pneumonia in some cases of diphtheria. 
However, bacteria have not been found in the lesions 1 in 
the heart and the process may therefore be properly con¬ 
sidered as a toxic myocarditis. The greater the amount of 
membrane and the longer the delay before sufficient anti¬ 
toxin is given, the more likelihood there is of serious involve¬ 
ment of the heart. 

Pathology. —This is of special interest because of the 
difference in opinion expressed in the literature as to 
whether any permanent damage remains in the hearts 
which have been seriously but not fatally involved. To 
quote one of the most exhaustive studies 1 of the condition, 
“Degeneration of the myocardium is one of the common 

1 Councilman, W. T., Mallory, F. B., Pearce, R. M.: “A Study of the 
Bacteriology and Pathology of Two Hundred and Twenty Fatal Cases of 
Diphtheria,” Jour. Boston Soc. Med. Sci., v: 139-319, 1900. 


165 



166 MODERN CONCEPTION OF HEART DISEASE 


conditions found in diphtheria. The simplest form of this 
is fatty degeneration, which is found in the majority of 
all cases. This varies in extent, at times affecting the 

myocardium generally, at times occurring in foci. 

The fatty degeneration accompanies and seems to precede 
the more advanced forms of degeneration which lead to the 

complete destruction of the muscle.Fragmentation 

and fracture of the degenerated muscle cells is often found 

.Simple fatty degeneration is found in the severe 

cases of short duration, the more extensive degenerations 
in the more prolonged cases. 

“Acute interstitial lesions of two sorts are found. In 
one there are focal collections of plasma and lymphoid 
cells in the tissue, which may be accompanied by degenera¬ 
tion of the myocardium, but are not dependent upon it. 
This condition is analogous to acute interstitial nephritis. 
In the other condition, the interstitial lesion consists of a 
proliferation of the cells of the tissue and is secondary to 
the degeneration of the muscle. It is probable that this 
may lead to extensive formation of connective tissue and 
some of the cases of fibrous myocarditis may be due to this.” 

Thrombosis due to primary necrosis of the endocardium 
is not uncommon. The post-mortem findings in cases 
showing high-grade heart-block have been recorded . 2 

Symptoms. —There is an initial acceleration of the 
heart rate to 130, 150, or more, and this usually subsides 
within forty-eight hours after the administration of anti¬ 
toxin. In about one third of the cases irregularities of the 
heart follow after the convalescence has been established 


2 Fleming, G. B., and Kennedy, A. M.: Heart, ii, 2: 77, 1910. 
Magnets-Alsleben, E. : Zeitschr. f . klin. Med., lxix:82, 1910. 
Price, F. W., and Mackenzie, Ivy: Heart, iii, 2:233, 1912. 







THE HEART IN DIPHTHERIA 


167 


about one week. According to the statistics of S. C. 
Smith, 3 85 per cent, of these arrhythmias are of simple 
nature, such as sinus arrhythmia, sino-auricular block, or 
premature beats. The remainder of the convalescent 
abnormalities were shown to be due to heart-block. 
The latter is often sudden in its onset and tends to 
become complete. 

A marked fall in the blood pressure occurs in the more 
severe cases. After a critical study of diphtheria, one 
observer 4 concludes that an essential feature is a decrease 
in the total volume of the blood and also an uneven distri¬ 
bution of the latter. As a result, the peripheral vessels 
may be almost empty. 

The patients in whom the serious heart lesions are pres¬ 
ent are usually those who were profoundly toxic when 
treatment was first instituted and in whom the initial 
tachycardia persisted for several days. They may be dull 
but fully conscious. The extremities are cold and the 
skin pale or sometimes slightly dusky. Pallor around the 
mouth is often present in such cases. Vomiting may occur. 
The pulse may be rapid and of poor quality, but when 
considerable heart-block is present the rate is usually sixty 
or below. Triple or gallop rhythm, perhaps indicating 
incomplete heart-block, may at times be noted. Death 
often results in one to two days. Embolism from the 
thrombi in the heart occurs occasionally. 

Auricular fibrillation is apparently rare, but has been 

3 “ Observations on the Heart in Diphtheria,” Jour. Amer. Med. Assn., 77, 
10:765, 1921. 

4 Harding, M. E.: The Circulatory Failure of Diphtheria, 1920, Univ. of 
London Press, Ltd. 



168 MODERN CONCEPTION OF HEART DISEASE 


recorded . 5 It occurred following complete heart-block 
and was permanent. In this case, also, the appearance of 
heart-block was delayed more than seven days after the 
onset of convalescence, in fact it was on the twenty-third 
day of the disease. Later in the convalescence, the pulse 
may be fairly normal in frequency but evidences a ten¬ 
dency to accelerate excessively on the least exertion, such 
as rising to the erect posture. This usually passes off in 
a few weeks. 

Diagnosis. —Normally there is a history of recent diph¬ 
theria. In any such condition as that of acute toxic heart- 
block, described above, the probability of diphtheria as a 
cause should be suggested and confirmed by the history, 
in case the latter was not known to the examiner. 

Prognosis. —The laryngeal type of diphtheria is less 
liable to be complicated by severe degeneration of the heart. 
Experience shows that the weakness of the heart, or other 
cardiac abnormalities, offer positive symptoms and physical 
signs during a period of sufficient duration to make their 
presence known. Thus patients rarely die suddenly, in 
a strict sense of the term. A persistence in the initial 
tachycardia and much evidence of toxicity are ominous. 
The cases showing severe cardiac symptoms on or after the 
sixth day usually die within a few days. In the experi¬ 
ence of E. H. Place , 6 the patients who survive heart-block 
for a week have a good chance of recovery, and deaths from 
this type never occur after two weeks. In by far the ma¬ 
jority of cases, if the patient survives the acute attack, 
the heart, after a few months, is perfectly normal, even to 

6 Parkinson, John: “ Auricular Fibrillation Following Complete Heart- 
Block in Diphtheria,” Heart, vi, 1:13, 1915. 

e Jour. Amer. Med. Assn., 77, 10:771, 1921. 



THE HEART IN DIPHTHERIA 


169 


electrocardiographic examination. Studies of the pathol¬ 
ogy, however, suggest the possibility of the replacement of 
some of the cellular elements by fibrous tissue. In Park¬ 
inson’s case, heart-block appeared on the twenty-third day 
of the diphtheria and auricular fibrillation followed on the 
thirty-third day. The heart-block eventually disappeared, 
but the fibrillation, of which electrocardiograms were 
repeatedly obtained, proved permanent. This is the only 
case, known to the writer, in which permanent damage to 
the heart seems conclusively established. 

Treatment. —Prevention is all-important by early and 
efficient use of antitoxin, intravenously if need be. It is 
foolish to wait for a positive culture if the clinical diagnosis 
of diphtheria is evident; at least one dose of antitoxin 
should be given. The aim is not to have the membrane 
shrivel and gradually come off in the course of a week or 
more, but it should be largely off within the first two or 
three days. 

Digitalis and other heart stimulants are of no benefit 
and may do harm. The only treatment that is of much 
value is that of absolute rest in as near the recumbent 
posture as possible. The rest must be prolonged so as to 
give the myocardium time to recover from the toxic degen¬ 
eration. Persistent vomiting may be met by allowing 
nothing by mouth, the injection of fluid by rectum, just 
enough to allay thirst, and the administration of morphia 
sufficient to keep the patient quiet and allay pain, if present. 


CHAPTER XIV 
CONGENITAL HEART DISEASE 

Cases of congenital heart disease are uncommon and 
often most complicated. The majority are defects in 
development, but a few are regarded as due to an infection 
of the endocardium and myocardium during fetal life. 
The signs and symptoms are so variable and the possible 
abnormalities in the heart are so numerous and bizarre 
that an accurate diagnosis is frequently impossible. 

Symptoms may be absent. Cyanosis is often present. 
It varies from a cyanosis that is limited to the lips, ears, 
etc., to one that is general. The skin may be almost purple, 
and of a far more intense color than occurs, with rare 
exceptions, in the cyanosis of acquired heart disease. The 
cyanosis associated with congenital heart disease is usually 
present at birth, the so-called blue baby. It is especially 
likely to be noted when emphasized at the time the baby 
has a spell of crying. Polycythemia with as many as eight 
or ten million red cells per cubic millimetre of blood may 
occur. Cough, dyspnoea, convulsions, bulging of the pre- 
cordium, and clubbing of the fingers and toes are common. 
Many cases show a tendency to epistaxis and to pulmonary 
tuberculosis. Congenital abnormalities elsewhere in the 
body may be associated. It should be remembered, how¬ 
ever, that any or all of the above symptoms may be absent. 

Some of the defects may be mentioned. 

Anomalies of Position. —1 . Dextrocardia is associ¬ 
ated with transposition of all the viscera. Symptoms are 
absent. The condition is commonly noted in the course of 

170 


CONGENITAL HEART DISEASE 


171 


routine examination, by the location of the apex impulse, 

percussion dulness, and maximum intensity of the heart 

sounds in the right chest, in an exactly similar relationship 

to each other as occurs in the heart normally located to 

the left of the sternum. Physical examination should 

%/ 

demonstrate that the liver and stomach have changed sides 
respectively. Rontgen examination will confirm the situs 
viscerum inversus of which dextrocardia is but one feature. 
The electrocardiogram, in a case of congenital dextro¬ 
cardia, shows an inversion of all waves in lead I, in which 
it differs from that of a heart displaced to the right by 
pleural exudates, pneumothorax, tumors, inflammatory 
processes in the chest, etc. The acquired form may be 
differentiated by the absence of evidence of associated 
transposition of the abdominal viscera. 

2. Ectopia cordis .—The cervical form is found only in 
the fetus. The heart may be located below the diaphragm. 
An imperfect closure of the parietes of the chest is some¬ 
times present in the pectoral form of ectopia cordis. 

Pulmonary Stenosis. —This is the most common type 
of congenital defect in the heart. The stenosis may be at 
the level of the pulmonic valve or below, at the junction 
of the conus arteriosus and main cavity of the right ven¬ 
tricle. In many cases the interventricular septum fails 
to close in its upper part, and in addition the ductus arteri¬ 
osus remains open. These latter defects serve somewhat 
to offset the pulmonary stenosis and the patient may have 
relatively few symptoms, whereas when pulmonary ste¬ 
nosis exists alone, the symptoms are pronounced and the 
patients rarely live over a year. 

The diagnosis is based on evidence of enlargement of 


172 MODERN CONCEPTION OF HEART DISEASE 


the right ventricle, and a systolic murmur and thrill of 
maximum intensity over the second left costal cartilage. 
The murmur may be transmitted to the neck, especially if 
the ductus arteriosus is patent. 

Caution should be used in assessing a systolic murmur 
and even thrill over the pulmonic area, in the absence of 
other signs or symptoms of abnormality. This is especially 
true in young babies. Thayer and MacCallum 1 have 
shown that it is extremely easy to produce both a murmur 
and thrill by light pressure on the infundibulum or pul¬ 
monary artery. Such a murmur and thrill commonly are 
much lessened or absent on inspiration. It is not unusual 
to observe the gradual disappearance of a systolic murmur 
over the second left interspace. The relationship of the 
vascular structures to the chest wall and the presence, in 
the infant, of the thymus gland, are the probable objects 
which exert external pressure and cause this innocu¬ 
ous murmur. 

Pulmonary Regurgitation 2 is rare. 

Patent Foramen Ovale. —A small opening in the 
interauricular septum is a common finding at autopsy in 
the essentially normal heart. In such cases signs and 
symptoms are absent in life. If a larger defect is present, 
signs and symptoms are usually present. The latter may 
be severe, especially when, as is often the case, the patent 
foramen ovale is associated with other abnormalities. The 
murmur attributed to non-closure of the foramen ovale 
may be systolic or both systolic and diastolic. These mur¬ 
murs are audible over the second, third, and fourth inter- 

1 Thayer, W. S., and MacCallum, W. G.: Amer. Jour. Med. Sci., 
cxxxiii: 249, 1907. 

2 Cautley, E.: Brit. Jour. Child. Dis., London, Oct.-Dec., 1920, 17, Nos. 
202-204, 187. 



CONGENITAL HEART DISEASE 


173 


costal spaces and are not transmitted to the neck. Patency 
of the foramen ovale makes possible the rare “crossed or 
paradoxical embolism,” for example an embolus to the 
brain from venous thrombosis of the leg. 

It seems fallacious to believe that the successful closure 
of the foramen ovale is in any way dependent upon the 
position in which the baby sleeps during the first two weeks 
of life. The valve-like fold or membrane, if present, will 
be kept in contact with the margin of the foramen by the 
greater pressure existing in the left auricle after birth. 
This increase in the left intra-auricular pressure is a natural 
result of the assumption of the pulmonary circulation. 

Perforate Interventricular Septum is a frequent 
defect, and, as said above, is often associated with pulmo¬ 
nary stenosis. The signs may resemble those of mitral in¬ 
sufficiency. A loud systolic murmur, not transmitted to the 
neck, may be heard over the third and fourth interspaces 
to the left of the sternum. Precordial bulging may 
be present. 

Patent Ductus Arteriosus (ductus Botalli).—The 
pulmonary artery is frequently dilated, which may be 
recognized by dulness in the second left interspace, with a 
pulsation, thrill, and loud systolic murmur which may reach 
the vessels of the neck or the fourth dorsal vertebra. Exces¬ 
sive dilatation of the pulmonary artery has been said to 
have compressed the recurrent laryngeal nerve, with sub¬ 
sequent hoarseness. In contrast to pulmonary stenosis, the 
pulmonic second sound is usually clear. An interesting 
point is that the Corrigan pulse and capillary pulsa¬ 
tion have been reported 3 as frequently associated with 
this defect. 


4 Walker, R. W. S.: Heart, ii, 3:249, 1911. 




174 MODERN CONCEPTION OF HEART DISEASE 


Coarctation of the Aorta or persistence of the isth¬ 
mus of the aorta. This is located in the posterior part of 
the aortic arch, and usually involves the extremity of the 
fifth left branchial arch, from which the ductus arteriosus 
is derived. A fibrous cord may connect the arch and the 
descending aorta, or a complete separation may exist. In 
such cases, the blood is delivered by the development of a 
collateral circulation; the upper intercostal arteries from 
the second part of the subclavian may communicate with 
the first aortic intercostal, also branches of the thyroid axis 
and the internal mammary arteries may do the same. This 
condition may exist in an adult and should be suspected if 
enlarged and tortuous arteries are detected on the back of 
the abdomen. 

A similar but rare malformation is an obliteration of the 
aorta just beyond the origin of the left subclavian artery. 
In this case the ductus arteriosus usually supplies blood 
to the descending aorta. 

Aortic Stenosis is uncommon. A systolic murmur 
and thrill, of maximum intensity at the second right costal 
cartilage, and transmitted towards the neck, are produced. 
As other anomalies, such as septal defects and patent 
ductus arteriosus, are usually associated, there may be 
other murmurs present, and the heart varies as regards the 
predominance of left or right ventricle. 

Treatment. —Congenital cardiac defects cannot be 
removed. Good hygiene and the avoidance of physical 
and mental strain are indicated. Treatment is largely 
symptomatic. Digitalis has but little place. If evidence 
of cardiac embarrassment is absent, the patient should 
lead an essentially normal life. 


CHAPTER XV 

EFFORT SYNDROME: IRRITABLE HEART 


The condition designated by the above title appears in 
the literature under various terms, such as, “irritable 
heart,” “cardiac neurosis,” “nervous heart,” “neuro-circu- 
latory asthenia,” “functional heart disease,” etc., and in the 
army parlance as, “soldier’s heart,” and “D.A.H.” ( i.e 
disordered action of the heart). Much emphasis was placed 
upon effort syndrome in the World War, but Jacob M. 
EaCosta, 1 as a result of observations made on soldiers of 
the American Civil War, clearly described the condition 
in 1871 under the designation of the “irritable heart of 
soldiers.” No term as yet seems entirely satisfactory; the 
double title used above serves to emphasize two of the more 
common types. The characteristic feature of effort syn¬ 
drome or irritable heart is that, in the absence of evidence 
of true cardiac disease, symptoms associated with physical 
effort occur out of proportion to the slight amount of 
physical exertion or emotional excitement required to 
excite them. 

Etiology. —Many cases may properly be attributed to 
recent or still present infections. In some, the condition 
seems to have a constitutional background, as a lack of 
good physical development. A sedentary life is a predis¬ 
posing factor. In others, nervous influences predominate. 
It has been thought that some degree of hyperthyroidism 
might be the cause, but careful studies appear to have 
shown that such is not the case. Physical exercise, in 


1 DaCosta, J. M.: Amer. Jour. Med. Sci., Ixi: 17, 1871. 


175 




176 MODERN CONCEPTION OF HEART DISEASE 


excess of the powers of the individual, and psychic strains 
will produce the symptom complex in the predisposed. 
The importance of infection in the causation of this dis¬ 
turbance should not be forgotten. 

Symptoms and Signs. 2 —The chief symptom is rapid 
heart action usually attended by precordial pain, shortness 
of breath, dizziness, and ojipression. The general appear¬ 
ance varies from healthy to florid or pallid. Tremors of 
the hands are common. The hands, in some cases, are cold 
and clammy and may be cyanotic, especially when they are 
in a dependent position. The pulse tends to be small and 
compressible. The blood pressure findings are inconstant. 

The heart rate is usually somewhat over 100 and is 
readily increased by exercise or excitement, i.e it is an 
unstable tachycardia. Sinus arrhythmia is not uncommon. 
The respirations are not accelerated in proportion to the 
pulse rate. 

Enlargement of the heart does not occur. On pal¬ 
pation, some degree of hyperesthesia of the precordia is 
present in nearly all who complain of recent severe pain. 
At times the latter may radiate down the left arm similarly 
to angina pectoris. A systolic murmur may often be noted 
modifying the first heart sound at the apex. In other 
cases, the first sound is described as split, or shortened, 
while the pulmonic second sound is often very distinct. 
None of these findings, it will be seen, are those of true 
cardiac disease. 

When the patient is in bed or kept sufficiently quiet 

2 If he has not already done so, the reader should read the excellent book by 
Thomas Lewis, The Soldier’s Heart and the Effort Syndrome, Paul B. 
Hoeber, New York, 1919. 



EFFORT SYNDROME: IRRITABLE HEART 


177 


and free from excitement, the above symptoms usually 
disappear completely or in a large measure. 

Diagnosis. —The presence or production of the symp¬ 
toms and signs normally associated with physical exercise, 
out of proportion to the exertion to which the patient has 
been subjected, and the absence of definite evidence of 
heart disease, should suggest effort syndrome or irritable 
heart. If the patient is of inferior physique, has incurred 
some recent infection, or has been subjected to undue 
physical or emotional strain, the diagnosis becomes increas¬ 
ingly probable. Care should be taken to exclude rheu¬ 
matic or syphilitic heart disease. 

Paroxysmal tachycardia should be differentiated by 
the fact that it occurs in attacks, with a sudden ending, and 
the rate remains essentially unchanged regardless of change 
in posture, etc. It is in no sense an unstable tachycardia. 

The heart in hyperthyroidism presents perhaps the 
most difficult problem in differential diagnosis. Decision 
should be reserved until the patient has been thoroughly 
examined and sometimes until the effect of treatment has 
been observed. Simple rest, or the recumbent posture, will 
usually quickly lower the pulse rate, whereas in true hyper¬ 
thyroidism, there is a tendency for some degree of tachy¬ 
cardia to persist even in sleep. When doubt remains, the 
result of the determination of the rate of the basal metab¬ 
olism is decisive. 

Prognosis. —Much depends on the probable cause. If 
the latter is an infection, its effects may usually be expected 
to wear away. A large proportion of the patients in whom 
hyperesthesia of the precordia is present are unable to 
12 


178 MODERN CONCEPTION OF HEART DISEASE 


perform any but the simplest exercises. 3 Marked breath¬ 
lessness and very high heart rates tend towards an unfa¬ 
vorable prognosis. If the patient is young and lacking in 
physical development, graded and systematic exercise may 
succeed in totally relieving the condition. In the older 
patients, or in those whose co-operation is less satisfactory, 
not so much should be expected from physical therapy. 
Considerable depends in the individual case as to what sort 
of occupation he is to follow or in what environment he is 
to live. 

Some conception of the prognosis in well-treated cases 
may be gained from noting the results in the British army. 
The disposition of these men on discharge from the hospital 
was as follows: 4 Fit for general service 20 per cent., fit 
for hardening or labor 30 per cent., fit for light or seden¬ 
tary work 30 per cent., and permanently unfit 20 per cent. 
The average length of stay in hospital had been six to 
ten weeks. 

Treatment. —The indication is clear to treat the pa¬ 
tient and not his heart. Search should be made for a focus 
of infection and, if present, measures should be instituted 
to free the patient from its influence. 

Time should be taken to make it clear to the patient 
that true heart disease is not present, and to obtain his co¬ 
operation in carrying out the treatment. A systematic 
course of training, starting with exercise sufficiently light 
and short for the individual patient and gradually increas¬ 
ing, will often be of much benefit. These measures can 
be employed more satisfactorily, it is true, when patients 

3 Meakixs, J. C., Gunson, E. B.: “The Occurrence of Hyperalgesia in the 
‘Irritable Heart of Soldiers,’” Heart, vi:343, 1917. 

* Lewis, Thomas: The Soldier’s Heart and the Effort Syndrome, p. 94. 



EFFORT SYNDROME: IRRITABLE HEART 


179 


are handled in groups, as was done in the army, but results 
can be obtained even with single cases if sufficient time and 
attention is applied. The patient, in some cases, should be 
warned that at first he may experience attacks of dizziness 
or palpitation, and if so he should be neither discouraged 
nor alarmed, but should rest from one half to two minutes 
and then try again. In a few days, in successful cases, 
the tendency to untoward symptoms will lessen, and thus 
the vigor and duration of the exercise may be increased until 
the patient works back to a condition of physical fitness. 

The patients in whom psychic stimuli are the apparent 
cause of the symptoms of an irritable heart are to be 
treated by the measures suitable for neurasthenia. The 
physician should obtain sufficient acquaintance with the 
patient’s environment and philosophy of life to enable him 
to point out things that may properly be avoided and the 
methods by which the patient may achieve greater ner¬ 
vous stability. 



































SECTION III 


FUNCTIONAL CONDITIONS 





CHAPTER XVI 
FUNCTIONAL CONDITIONS 

In the preceding chapters, frequent reference has been 
made to heart failure, angina pectoris, and the various 
arrhythmias. These conditions will now be presented in 
the above order. It is emphasized that they should not be 
considered complete entities; they are merely functional 
conditions which may be associated with the several types 
of heart disease. 

HEART FAILURE 

The term “broken compensation” has long been em¬ 
ployed for this condition. However, since the explanation 
of cardiac embarrassment on the basis of mechanical effects 
has been largely abandoned in favor of infection as a cause, 
“failure of compensation,” with its implication of hyper¬ 
trophy, seems less desirable. Symptoms of heart failure 
may appear in a paroxysm of tachycardia in which no 
hypertrophy has ensued. 

Heart failure may be said to be present when there 
are a certain set of symptoms and signs that are untoward 
for the patient under examination. The picture is not 
unlike that which may be produced in large part in a healthy 
individual when exercise is pushed to the physiological 
limit and beyond, but it is present in the patient with heart 
disease while at rest, or as a result of exertion insufficient 
to call it forth in health. 

The first indications are symptoms, such as pain, breath¬ 
lessness on exertion, and undue fatigue. The tolerance of 

183 


184 MODERN CONCEPTION OF HEART DISEASE 


exercise is reduced; this statement should be checked by 
the remarks on this in the chapter on Effort Syndrome 
and in that on Methods of Examination. Symptoms 
referable to the stomach are common. 

Heart failure with congestion is a familiar type. An 
important sign is an engorgement of the cervical veins. 
If the veins are distended when the patient is standing or 
sitting (care being taken to avoid pressure on the abdomen) 
it may be confidently stated that the pressure is raised in 
the veins. The right heart is enlarged, but it may be 
remarked that the results of percussion, etc., to detect this 
are equivocal. The evidence obtainable from the condition 
of the veins in the neck is more trustworthy. As the heart 
failure undergoes further development, the breathlessness 
increases, and cyanosis, rales at the pulmonary bases, swell¬ 
ing of the liver, edema of the legs, ascites, and a lessening 
in the urinary output, aj)pear. As stated elsewhere, seri¬ 
ous heart failure may exist without edema. Angina pec¬ 
toris is a form of heart failure, but it is sufficiently distinc¬ 
tive to demand separate presentation. 

The treatment and other details of heart failure are 
sufficiently considered in other parts of this book. 

ANGINA PECTORIS 

The term angina pectoris is applied to a condition char¬ 
acterized by attacks of pain over the heart, with a tendency 
to radiate to the left shoulder and arm, and often accom¬ 
panied by a sense of impending death. 

Etiology. —Males are more frequently affected. Cer¬ 
tain families are known to be prone to this affection. An¬ 
gina pectoris may occur at any age after infancy, but 
it is much more common in patients forty-five to fifty years 


ANGINA PECTORIS 


185 


of age or more. Excessive wear and tear of life are appar¬ 
ent factors. Increased weight, in the causation of angina 
pectoris, has of late been given to infectious diseases, espe¬ 
cially syphilis. Next in order comes influenza, then 
rheumatic fever, infections with the streptococcus, and 
occasionally other infections. The commonest conditions 
associated with angina pectoris are arteriosclerosis, syph¬ 
ilis, and chronic hypertension. 

Authorities are not agreed as to the pathological cause 
of angina pectoris. The view which perhaps has gained 
the widest acceptance is that the disease could be traced 
to sclerosis of the coronary arteries or to a spasm of these 
vessels causing an ischemia of the myocardium. More 
recently, however, an aortitis as the true lesion has gained 
many advocates. In view of the interest of the subject it 
seems proper to discuss briefly these leading theories. 

The coronary sclerosis theory does not explain the cases, 
now numerous, in which post-mortem examination has dis¬ 
closed normal coronary arteries. Also, doubt is thrown 
upon the importance of sclerosis of the coronary arteries 
since, in the age period in which angina pectoris is most 
frequent, arteriosclerosis is also common. In fact, in ne¬ 
cropsies conducted on elderly subjects, it is the rule to find 
some degree of coronary sclerosis associated with more 
general arteriosclerosis, and yet but comparatively few of 
these patients in life were afflicted with angina pectoris. 
The coronary arteries may be sclerosed almost to oblitera¬ 
tion without apparent damage to the myocardium, or 
symptoms during life. This is probably explainable by 
the establishment, provided the silting up of the coronary 
channels is slow enough, of compensatory circulation, by 


186 MODERN CONCEPTION OF HEART DISEASE 


means of the free anastomosis of the right and left cor¬ 
onaries. Also, Pratt 1 has pointed out that the veins of 
Thebesius may supply blood sufficient to maintain the 
integrity of the myocardium. 

If angina pectoris is not due to coronary sclerosis, then 
some say it is caused by attacks of claudication causing 
myocardial ischemia. As yet I am unaware of any data 
in proof of this conception. The accuracy of the analogy 
to claudication in the horse is open to question, as the horse 
so attacked limps, but it is not so with the heart during an 
anginal attack. The weight of evidence from the physio¬ 
logical laboratory makes it doubtful if a contraction or 
spasm of the coronary arteries ever takes place. 

Sir Clifford Allbutt 2 writes very compellingly in favor 
of the aortitis theory of angina pectoris. In brief, the 
condition is presumed to be due to irritation of the nerve 
end-plates in the first part of the aorta by the placques of 
an aortitis, and is especially liable to occur in conditions 
causing a rise of the intra-arterial pressure and subsequent 
stretching of the investing membranes of the root of the 
aorta. There may be a partial analogy to the pain caused 
by dragging on the mesentery. To quote from this dis¬ 
tinguished author: “Still, so far as I am aware, there is not 
a case of angina on record, on responsible authority, in 
which disease of the coronaries was the sole lesion; none, 
that is, in which, for instance, the state of the suprasigmoid 
aorta also had been histologically examined, within and 
without, and declared normal.” 

While the advocates of the aortic causation of angina 

‘Pratt, F. H.: Amer. Jour. Physiol., 1: 86, 1898. 

2 Diseases of the Arteries, Including Angina Pectoris, Macmillan & 
Co., Ltd., 1915. 



ANGINA PECTORIS 


187 


pectoris deny the coronary theory, they do believe that the 
condition of the coronary arteries and the myocardium is 
of importance in determining the survival or death of the 
patient experiencing the anginal attack. Thus, death is 
explained by reflex vagus inhibition of the heart, and fail¬ 
ure, in cases with poor myocardium, of the process of 
ventricular escape. It seems more likely, however, that 
death is due to the occurrence of fibrillation of the ventricles. 

Mackenzie writes 3 that he is uncertain of the exact cause 
of angina pectoris but considers some form of heart exhaus¬ 
tion, and treats it on that basis. In the opinion of the 
author, this is a wise and conservative position. 

An appreciation of the factors involved makes apparent 
the difficulties in the way of obtaining the data necessary 
to establish the etiology of angina pectoris. As yet the 
verdict must be “not proven,” and yet the above theories 
serve as important leads from which to base our thera¬ 
peutic measures. 

Symptoms. —Typical angina pectoris is characterized 
by paroxysmal attacks of pain over the sternum, often 
radiating to the left shoulder and arm, and commonly 
associated with a sense of impending death. 

The pain varies from a mere sense of uneasiness or con¬ 
striction to that of intense agony. Its location is under 
or near the sternum, particularly the upper portion. 
Allbutt points out that if the pain is precordial or near the 
nipple it is not due to angina pectoris but to some other 
affection of the heart, usually with failure. 

The pain in angina shows a distinct tendency to radiate 
to the left shoulder and arm. A favorite location is over 


3 Mackenzie, James: Oxford Medicine, ii, 387, 1920. 



188 MODERN CONCEPTION OF HEART DISEASE 


the area of the lesser internal cutaneous nerve. It is less 
common for the radiation to extend below the elbow, and 
when it does so, it is more likely to follow the ulnar than 
the median distribution. Radiation to the right upper 
extremity and to the neck occurs, but is less common. At 
times the pain may strike through to the region near the 
inferior angle of the left scapula or to a larger area in the 
back. Rarely the pain may be felt in the lower jaw or 
molar tooth. Epigastric and abdominal locations are occa¬ 
sionally described as occurring in angina pectoris, and have 
even been accompanied by jaundice. 

At times the pain may be absent over the sternum and 
present in one of the points of radiation. Thus patients 
may present themselves with the complaint of pain only 
in the arm or hand. Later on, these cases may develop 
typical angina pectoris. 

The attacks are commonly brought on by exertion, as 
by climbing an ascent or walking against the wind. Large 
meals may precipitate an attack; in fact, it is felt that many 
of the attacks and deaths from so-called “acute indiges¬ 
tion” are really due to angina pectoris. Sudden chilling 
of the body surface, as a cold shower or cold sheets, may 
induce a paroxysm. The discomfort or irritation of a dis¬ 
tended bladder, due to prostatic obstruction, may provoke 
the paroxysm. The attacks usually occur during the wak¬ 
ing hours, but occasionally may disturb the patient at 
night. Victims of angina pectoris are also prone to de¬ 
velop an attack following an emotional state, such as 
sudden rage. Thus, there is some foundation for the 
novelist’s tendency to dispose of an elderly character by 
sudden death after intense rage or joy. 


ANGINA PECTORIS 


189 


An indescribable sense of impending death often accom¬ 
panies an attack of angina. If present, it is of considerable 
diagnostic value. Often the patient will spontaneously 
mention this feeling, in more reticent individuals it may be 
elicited by suitable questioning. 

When seized by an attack of angina, the victim practi¬ 
cally always remains motionless. The patient, who may be 
walking at the time, will pause to look in a window or lean 
against a fence, and resume his course only after the attack 
has ceased. The respiration is never deepened, but is often 
shallow or temporarily suspended. It is common for the 
skin to pale markedly, and beads of perspiration may 
appear on the forehead. 

The pulse, to one’s surprise, may show practically no 
change. In fact, unless some other cardiac affection is 
present, no change will be noted in the pulse beyond an 
occasional elevation of the rate by a few beats. There is 
a slight divergence of opinion as regards blood pressure, 
but in the experience of the author, it shows no alteration 
in the peripheral pressure. 

Death may suddenly terminate the attack. 

Diagnosis. —Angina pectoris, it will be seen, is to be 
diagnosed from the history and symptoms, and not from 
physical signs. In well-marked cases, the agonizing pain, 
with its tendency to radiation, and accompanied by a sense 
of impending dissolution, clearly points to angina pectoris. 
But it is in the less-developed cases, where perhaps the 
pain is felt only at one of the points of radiation, or in the 
case in which the only symptom is an indescribable feeling 
of uneasiness over the sternum, that care should be taken 
not to treat the matter too lightly. Questions should be 


190 MODERN CONCEPTION OF HEART DISEASE 

directed to ascertain the circumstances under which these 
symptoms occurred, and, if there is evidence of syphilis or 
if the patient is beyond middle age, the possibility of angina 
pectoris should be considered. It should be mentioned 
here that angina pectoris appears in both severe and mild 
forms. Thus, if the symptoms are light, one is neverthe¬ 
less dealing with the same disease as if the patient were 
experiencing intense agony. 

The presence of other cardiac affections in which pain 
is a symptom may complicate the picture, especially if 
evidence of cardiac failure has appeared. But if the ob¬ 
server keeps clearly in mind the symptoms discussed above, 
he may yet be able to diagnose both conditions. 

True angina pectoris is to be distinguished from mock 
angina. The latter is held to be a vaso-vagal attack which, 
unlike true angina, is spontaneous in origin. Huchard’s 
well-known table (which I have modified somewhat) em¬ 
phasizes some of the contrasts. 

Allbutt writes of mock angina, as contrasted to true 
angina: “The pain is different, the pulse is different, the 
panting is different, the behavior is different, the storm is 
different, the duration is different, the causes are different, 
the issue is different.” 

The use of tobacco in excess may rarely cause mock 
angina. 

Occasionally thrombosis or embolism of the coronary 
circulation is to be differentiated. An acute pain may 
occur, but, unlike true angina, it may persist without abate¬ 
ment for twenty-four to thirty-six hours. It is commonly 
associated with a marked fall of blood pressure, dyspnoea, 
and pulmonary edema. Sir William Osier, and others, 


ANGINA PECTORIS 


191 


have pointed out, however, that even in cases of sudden 
death due to blocking of one of the coronaries, or a large 
branch such as the anterior, the seizure is usually painless. 
This fact and the marked fall in blood pressure, which 


Angina Pectoris 

Most common in men be¬ 
tween forty and fifty. 

Paroxysm induced by exer¬ 
tion, etc.: diurnal; few in 
number. 

Pain intense, of short dura¬ 
tion, substernal; sensation 
of cardiac compression. 

Patient inarticulate; immo¬ 
bile attitude; respiration 
shallow. 

Pulse unchanged. 

Nervous symptoms absent. 

Prognosis grave, often fatal. 

An aortitis, or stenosis of 
coronary arteries often 
present. 


Mock Angina 

Commonest in women, at 
any age. 

Spontaneous; often noc¬ 
turnal and periodic; fre¬ 
quent. 

Less severe, lasting hours; 
epigastric; sensation of 
distention. 

Agitation, and activity; res¬ 
piration often accelerated. 

Pulse often weakened. 

Neurasthenic or hysterical 
stigmata. 

Never fatal. 

No lesions found. 


also follows experimental ligation of the coronaries, ap¬ 
pears to throw further doubt on the theory of an ische¬ 
mia due to coronary claudication as the explanation of 
angina pectoris. 

Alteration in the ventricular complex in the electro¬ 
cardiogram may be observed. 4 


4 Pardee, H. E. B.: Arch. Int. Med., 26 : 244 (Aug., 1920). 



192 MODERN CONCEPTION OF HEART DISEASE 


Prognosis. —The prognosis should be guarded, as 
death is possible in the first or any subsequent attack. If 
heart failure ensues, the anginal attacks usually cease, but 
may reappear with improvement in the heart action. The 
late John H. Musser, Sr., emphasized that a change of 
physical type occurred in those patients in whom the 
appearance of cardiac failure was associated with the dis¬ 
appearance of the anginal attacks. That is, the vigorous, 
active individual soon took on the characteristics of the 
broken-down subject. 

If the angina is due to syphilis, considerable relief or 
even an arrest of the disease may result from timely treat¬ 
ment. Angina due to an infection other than syphilis 
tends to subside spontaneously. 

Treatment. —The treatment is directed towards the 
relief of the attack and the prevention of their repetition. 

For the attack, a rapidly acting vasodilator has been 
found most helpful. The inhalation of the fumes of a 
“pearl,” containing 5 min. (0.3 c.c.) of amyl nitrite, freshly 
crushed in the handkerchief, gives quickest relief. Nitro¬ 
glycerine, however, is generally the more satisfactory rem¬ 
edy and is preferred by most of the patients. A tablet, 
gm. 0.006 ( Vioo gr.), allowed to dissolve under the tongue, 
should act in about three to five minutes. The same 
amount may be repeated in ten minutes if relief has not 
been obtained. In some individuals, it may be necessary 
to work up to a much larger dosage. 

Morphine, gm. 0.01 to 0.015 (V 6 to V 4 gr.), is a sov¬ 
ereign remedy in a severe attack and has the added benefit 
of ensuring a quiet patient for several hours. 

Heat, in the form of a hot-water bag, electric pad, etc., 


ANGINA PECTORIS 


193 


may be applied to the precordium. The patient ought 
properly to be kept at rest for several days, as it has been 
noted that there is a tendency for attacks to occur in cycles, 
and the attack may be repeated. 

As it is only occasionally that the physician is present 
at the time of the attack, the patient or a member of the 
family should be carefully instructed in the treatment of 
the acute attack. If the physician or other responsible 
person is present during the paroxysm, the nitroglycerine 
or morphine may be given hypodermically. 

Between attacks, attention should be paid, primarily, 
to therapy based on a study of the case from an etiological 
viewpoint. It is especially important that antisyphilitic 
treatment be given whenever indicated, and some would 
say it should be given a trial in each case. If it is decided 
that arteriosclerosis is the causative factor, the treatment 
pertaining to that disease is indicated. Occasionally the 
underlying condition is hypertensive heart disease, for 
which appropriate therapy should be instituted. 

The conditions predisposing to attacks of angina pec¬ 
toris should be explained to the patient, so that they may, 
if possible, be avoided. These are: exertion, excitement, 
worry, chilling, sexual intercourse, constipation, dyspepsia, 
late suppers, large meals, and foods favoring flatulency. 
If there is a tendency to gastric flatulency, the patient 
should be provided with some aromatic, as Hoffman’s ano¬ 
dyne (Spiritus .ZEtheris Compositus), or some mixture as: 

Spiritus ammonise aromatici 

Spiritus chloroformis 

Spiritus astheris compositi aa, 5 i ss. 

Sig .: To be taken in hot water. 


13 


194 MODERN CONCEPTION OF HEART DISEASE 


In elderly men, with hypertrophied prostates, measures 
should be taken to avoid bladder distention. 

The use of nitroglycerine 0.006 gm. (Vioo gr.) three 
times a day, as sometimes prescribed, is problematical, as 
the action of the drug is less than one hour in duration. 
If a more continuous action of a vasodilator is desired, 
nitroglycerine should be repeated at frequent intervals, 
or sodium nitrite 0.06 gm. (1 gr.), or erythrol tetranitrate 
0.03 to 0.06 gm. (y 2 to 1 gr.) every three to four hours, 
should be substituted. It has often been proven of value, 
however, to advise the patient to take his dose of nitro¬ 
glycerine just before any known physical exertion, as a 
walk to the store, etc., in order to ward off an anginal attack. 

Good results have also been obtained from the swallow¬ 
ing of the nitroglycerine already in solution. It should 
be remembered that, to be active, the drug should be fresh, 
and it is, therefore, a wise precaution for the patient to 
renew weekly the emergency supply of nitroglycerine that 
is carried on his person. For those who hesitate to pre¬ 
scribe nitroglycerine, due to uncertainty as to its toleration 
by the patient, it is suggested that gr. Vioo of the drug be 
administered as a test while the patient is yet in the office. 


CHAPTER XVII 
THE ARRHYTHMIAS 

A large part in the recent advance in the subject of 
heart affections has come from the studies of normal and 
abnormal cardiac function. The use of graphic methods 
of examination has contributed greatly, with but few excep¬ 
tions, to the elucidation of the nature of irregular or dis¬ 
ordered mechanism of the heart. Now that the essential 
facts have been established, it is found that the arrhythmias 
may often be correctly diagnosed without resort to the 
use of the polygraph or electrocardiograph. Since the con¬ 
tributions of the polygram and the electrocardiogram have 
been described, briefly it is true, in earlier chapters, in the 
following, the chief features of the various arrhythmias will 
be presented from the standpoint of observations made by 
the more usual clinical methods. Attention is drawn to 
the fact that the arrhythmias are not true entities in the 
sense that are rheumatic heart disease, cardiovascular 
syphilis, etc.; these functional conditions may be features 
of various heart affections. 

SINUS ARRHYTHMIA 

In sinus arrhythmia the impulse from the pacemaxer of 
the heart ( i.e the sino-auricular node) starts irregularly 
and causes thereby an arrhythmia of the whole heart. 

It is due to variation in the control of the heart by the 
vagus nerve. The usual type is that in which the heart 
accelerates with inspiration and slows with expiration, but 
the conditions may be reversed. A much less frequent 

195 


196 MODERN CONCEPTION OF HEART DISEASE 


form of sinus arrhythmia is phasic irregularity, in which the 
whole heart slows periodically and not in relation to res¬ 
piration. Respiratory irregularity of the heart rhythm 
is present in almost all children. After the age of puberty, 
it rapidly becomes less common, and in adults is inconspicu¬ 
ous or absent save in forced breathing. Respiratory vari¬ 
ations in the pulse rate are often conspicuous during 
convalescence from acute illnesses. 

Sinus arrhythmia causes no symptoms. It is usually 
detected solely as the result of physical examination. In 
most cases it may be considered physiological. If it has 
appeared in an adult during convalescence from some feb¬ 
rile disease, it will often diminish or disappear in a few 
weeks or months. 

No treatment is needed. It may be temporarily abol¬ 
ished by the action of atropine. 

It is important that the nature of sinus arrhythmia be 
understood, as it may cause unnecessary alarm on the part 
of physician and patient. 

SINO-AURICULAR BLOCK 

Sino-auricular block may resemble the form of heart- 
block showing dropped beats. Its presence should be sus¬ 
pected in patients in whom, especially after exercise, the 
heart rate slows gradually to 80 or 70 and then drops to 
about one half. It may result from digitalis administra¬ 
tion; in some cases it is associated with respiration. It 
appears closely related to sinus arrhythmia and to the 
action of the vagus nerve. Sino-auricular block is often 
associated with auriculo-ventricular block. The hypoth¬ 
esis of a lesion or condition causing a block between the 


THE ARRHYTHMIAS 197 

sinus node and the auricular tissue lacks anatomical or 
physiological proof. 

Sino-auricular block is commonly symptomless. Its 
presence does not imply disease. When due to digitalis, 
it will disappear on the discontinuance of the drug. No 
treatment is required. 

This arrhythmia is relatively uncommon and is rarely 
diagnosed save as a result of examination by the graphic 
methods. 

PREMATURE BEATS OR EXTRASY'STOLES 

Premature beats or extrasystoles are very common; in 
fact, their prevalence is so great that it is suggested that 
all patients are subject to them at some time. They may 
arise in the auricle or in the ventricle, being five times as 
frequent in the latter. Auricular premature beats are, 
however, more important, as they are often associated 
with paroxysmal tachycardia. 

Etiology. —The causation of extrasystoles is obscure. 
They are premature beats of the heart in response to stim¬ 
uli, probably newly generated, and not forming part of 
the rhythmic series of contractions. Their point of origin, 
save for rare exceptions, is in some part of the myocardium 
other than the sino-auricular node. It is commonly held 
that they are evidence of increased excitability of the car¬ 
diac tissues, but according to Lewis , 1 that is pure hypoth¬ 
esis. Premature beats may at times be associated with 
the action of certain poisons, such as: chloroform, digi¬ 
talis, strophanthin, aconitine, barium chloride, potassium 
salts, nicotine, theophyllin, muscarine, and physostigmine, 

1 Lewis, Thomas: The Mechanism and Graphic Registration of the Heart 
Beat, Paul B. Hoeber, N. Y., 1920, p. 342. 



198 MODERN CONCEPTION OF HEART DISEASE 


tea, coffee; and with certain conditions, as: toxemia, ner¬ 
vousness, arteriosclerosis, syphilis, and hypertension. 

While their incidence is most frequent in patients in 
whom there is structural disease of the heart, their preva¬ 
lence amongst apparently healthy people largely destroys 
the significance of this relation. 

Symptoms and Signs are often absent. Occasionally 
the patient is conscious of the cardiac irregularity and 
states that it feels as though the heart “turned over.” 
Palpitation may be present. Breathlessness on exertion 
may be noted in the occasional patients exhibiting extra¬ 
systoles at a high rate of the heart. 

The heart rate is usually under 100, and the premature 
beats will disappear if the rate is accelerated to over 110. 
Rare exceptions to the above statement occur; the writer 
has electrocardiograms showing frequent auricular prema¬ 
ture beats even at the cardiac rate of 146 per minute. 

On auscultation of a typical case, it is easy to detect 
the prematurity of the extrasystoles and the succeeding 
pause. One or two sounds will be audible, according as 
the extrasystole is strong enough to open the semilunar 
valves (second sound results from their closure). Whether 
the extrasystole will be represented in the radial pulse 
depends upon the amount of blood expelled by the heart. 
A series of rhythmic heart sounds, interrupted by one that 
is premature, should at once suggest an extrasystole, but 
when the irregular beats are frequent, it may be necessary 
to resort to some method to accelerate the heart rate (un¬ 
less it is already elevated), and the irregular beats should 
diminish or disappear. 

If the pause following the premature beat is not fully 


THE ARRHYTHMIAS 


199 


compensatory, it may confidently be asserted that the beat 
was of auricular origin , 2 while if a fully compensatory 
pause is present, the ectopic beat almost certainly comes 
from the ventricular tissue (with rare exceptions). 

Differential Diagnosis. —Premature beats are to be 
distinguished from fibrillation of the auricles. This is 
usually evident at once. A rule that has rare exceptions 
is, that premature beats diminish or disappear following 
acceleration of the heart rate, as by exercise. When the 
arrhythmia is due to extrasystoles, the irregularity is not 
absolute; the prematurely occurring beats are nearly 
always followed by a pause of increased length. In fibril¬ 
lation, the post-systolic pauses are unrelated to the time 
of occurrence of the beats. The ventricular type of venous 
pulse may be observed in fibrillation, but not in extra- 
systolic arrhythmia. 

Incomplete heart-block, causing dropped beats, is 
readily confused with premature beats, due to the fact that 
the latter are often not transmitted to the wrist. The 
desirability of avoiding this mistake is obvious, since the 
two conditions differ widely in prognosis and treatment. 
Extrasystoles are common and dropped beats of relatively 
rare occurrence. It is unsafe to diagnose a dropped beat, 
and so heart-block, from evidence obtained solely by pal¬ 
pation of the pulse. This latter diagnosis ought properly 
to be confirmed by the use of the graphic methods of exam¬ 
ination. On auscultation at the apex, the extrasystole may 
show two heart sounds, but in case merely a single faint 
sound is audible, this must be differentiated from the occa¬ 
sionally faintly audible sound of the auricle, the contraction 

3 Rare exception: idio-ventricular rhythm interrupted by ventricular 
extrasystoles. 



200 MODERN CONCEPTION OF HEART DISEASE 


of which now occurs during the period when the heart 
should be silent. More often the condition of dropped beat 
is represented on auscultation by a gap in the heart sounds. 
The absence of symptoms of heart failure and the prompt 
disappearance of the irregularity, on acceleration of the 
heart rate by exercise, are strongly in favor of the simpler 
diagnosis, namely premature beats. However, after accel¬ 
eration of the pulse by exercise, the irregularity, due to 
either premature beats or the dropped beats of heart-block, 
may completely disappear, and then, as urged by Lewis , 3 
particular attention should he directed to the first irregu¬ 
larity that appears as the pulse rate falls. If the arrhyth¬ 
mia is due to premature beats, a premature beat will be 
heard, while there will be a gap if heart-block is the cause. 

Prognosis. —The presence of premature beats without 
other evidence of cardiac abnormality is of little prognostic 
import. They may come and go, or persist for years, with 
no evidence of physical impairment. 

Treatment. —The detection of the premature beats 
should indicate the need of investigation sufficient to dis¬ 
cover the presence or absence of evidence of heart disease, 
and any of the conditions, mentioned above, which have 
been found in association with this arrhythmia. These 
associated conditions, or apparent causes, should be re¬ 
moved if possible. Other than this, most cases affected 
by extrasystoles require no treatment. 

When symptoms are present, and especially in the occa¬ 
sional patient in whom the premature beats persist at the 
higher cardiac rate, the temporary use of bromides and 
veronal may be of assistance. 

3 Lewis, T.: The Soldier’s Heart and the Effort Syndrome: Paul B. Hoeber, 
New York, 1919, p. 72. 



201 


THE ARRHYTHMIAS 

PAROXYSMAL TACHYCARDIA 

This is definable as tachycardia of regular rate, and 
sudden onset and cessation. It is of auricular origin about 
twenty times as frequently as it is ventricular. This de¬ 
scription will be limited to the auricular type. 

Etiology. —Paroxysmal tachycardia has been noted as 
early as the age of six, and as late as seventy-four years; 
the period of twenty to forty is the commonest. It occurs 
in females and males in about the proportion of three 
to two. 

The apparent causes are essentially the same as in the 
case of premature beats (which see). Those who accept 
the hypothesis that extrasystoles are due to increased ex¬ 
citability of the heart consider that paroxysmal tachy¬ 
cardia indicates a somewhat higher degree of excitability. 

The mechanism is obscure. Evidence obtained by the 
graphic methods of examination discloses that a paroxysm 
is introduced by a premature contraction, and apparently 
is a series of the latter repeated in rapid and regular suc¬ 
cession. What is not clear, is, how it comes about that 
these new impulse centres, which commonly have the power 
to build up a stimulus at a relatively low rate (usually 
below 100), can suddenly produce a series in rapid succes¬ 
sion. Now that it has been established that auricular flut¬ 
ter (which see) is due to circus movement, the hypothesis 
of a similar mechanism, leading to the production of parox¬ 
ysmal tachycardia, is very tempting. 

Pathology. —This is unknown in mild cases, as they 
are not examined; in some instances myocardial changes 
have been found. 

Symptoms and Signs. —Exertion or excitement usu- 


202 MODERN CONCEPTION OF HEART DISEASE 


ally start the paroxysm, which rarely persists for more 
than a few hours, though it may continue for several weeks. 
A duration of a few minutes or seconds is not uncommon; 
exceptionally long and short attacks may occur in the same 
patient. The condition is felt by the patient as palpita¬ 
tion. There may be dyspnoea and some precordial or epi¬ 
gastric distress. The sensation of pounding on top of the 
head is at times most unpleasant. In the paroxysms of 
long duration, the liver may swell and all the signs of 
cardiac failure be in evidence. 

The pulse rate is commonly over 140 to the minute and 
under 200, which figure is arbitrarily set to separate parox¬ 
ysmal tachycardia from flutter of the auricles. A striking 
feature is the regularity of the rate, and that it is hardly 
affected by change of posture, though Lewis 4 has reported 
a variation as high as twelve beats between the rate on 
standing and on lying. In addition to the rapid rate, the 
volume of the pulse is often small and subject to consider¬ 
able respiratory change. The size of the heart during a 
paroxysm was diminished when examined radioscopically 
by Vaquez and Bordet; 5 in a persistent attack, dilatation 
of the heart may ensue. 

Diagnosis. —This is usually evident from the presence 
of a regular tachycardia, less than 200 to the minute, and 
but slightly affected by change of posture. The use of 
graphic methods is helpful on the doubtful cases. 

It is more often the case, however, that the patient is 
seen between attacks, and then the diagnosis must perforce 

4 Lewis, T.: The Mechanism and Graphic Registration of the Heart Beat, 
Paul B. Hoeber, New York, 1920, p. 244. 

5 Vaquez, H., and Bordet, E.: Le Coeur et I’Aorte, J. B. Bailliere et Fils, 
Paris, 1920, p. 155. 



THE ARRHYTHMIAS 


203 


rest upon the history. Of particular value is a positive his¬ 
tory of an abrupt beginning and ending of the attacks, the 
rate and regularity of the heart during the “palpitation,” 
and the association of vomiting with the ending of an 
attack, or the details of any of the measures by which the 
patient may have learned to terminate the paroxysm. 

The tachycardias due to hyperthyroidism and to the 
effort syndrome or irritable heart should be differentiated 
by the fact that they in no sense possess the remarkable 
regularity in rate, or the abrupt onset and cessation, so 
characteristic of paroxysmal tachycardia. 

The distinction from auricular flutter is based upon the 
tendency of the latter to show a greater degree of heart 
failure and to be permanent. An electrocardiogram 
should settle the doubt. The matter will be further dis¬ 
cussed under auricular flutter. 

Prognosis. —This is usually good in the short and 
early attacks. If the paroxysm is of the persistent type, 
occasionally grave heart failure and death may result. 
The prognosis is influenced, of course, by evidence of other 
abnormality of the heart. 

Treatment. —The attack may be promptly termi¬ 
nated, in a considerable portion of the cases, by resort to 
procedures which produce stimulation of the vagus nerve. 
The latter is accessible in the neck where the right and left 
trunks course downward in the posterior part of the respec¬ 
tive carotid sheaths, and may be stimulated by compressing 
the artery, at the level of the cricoid cartilage, between the 
ball of the thumb and the vertebral column. The pressure 
should be sufficient to obliterate the carotid pulsations, and 
should be continued 15 to 20 seconds. This manoeuvre 


204 MODERN CONCEPTION OF HEART DISEASE 


should be performed first in the right neck, and, if the 
tachycardia persists, should then be earned out over the 
left carotid. Support of the patient’s neck, from behind, 
by the opposite hand, is often helpful. Sometimes success 
comes only after repeating, two or three times, the above 
method of stimulation of the vagus. Untoward results, 
i.e., convulsions from cerebral anemia, have sometimes 
followed the simultaneous compression of both vagi. 

If the paroxysm is uninfluenced by pressure on the 
vagus in the neck, the nerve may be stimulated by pressure 
for a similar duration on the eyeballs, through the closed 
lids. Since this procedure readily causes pain to conscious 
patients (some cases occur while under surgical anes¬ 
thesia), not more than moderate pressure can usually 
be tolerated. 

A change in the position of the patient, such as bending 
well over, has helped. Drinking ice-cold water has re¬ 
lieved some patients. Deep breathing, and the holding of 
a deep breath, may be tried. The induction of vomiting 
by ipecac, or by inserting the finger in the throat, has ter¬ 
minated many attacks. An abdominal belt, or firm pres¬ 
sure on the abdomen, has proven successful at times, 
perhaps due to flushing of the heart by the return of an 
extra amount of venous blood. 

If the attack continues, an ice bag to the precordia is 
indicated. Digitalis should be employed in persistent 
cases, but one should not rush to this treatment. 

Between the attacks, the important measures are, first, 
rest, and then to avoid the apparent exciting cause, as 
excitement, exertion, and heavy meals, etc. Bromides and 
veronal may be of service where nervous factors are 
prominent. 


205 


THE ARRHYTHMIAS 
AURICULAR FLUTTER 

This may be defined as a condition in which the auricle 
beats regularly at a rate averaging about 300 per minute. 
It is a relatively rare cardiac rhythm. 

Etiology. —Auricular flutter may be present as early 
as the age of five, and in advanced years; the most frequent 
period is forty to sixty years. Among the conditions 
associated with flutter are arteriosclerosis, coronary scle¬ 
rosis, rheumatic heart disease, and syphilis. Nervousness 
appears to be much less of a factor than it is in paroxysmal 
tachycardia. 

The mechanism of flutter of the auricles would seem to 
have been established in 1920, by Lewis and his collabora¬ 
tors. * * 6 These authors demonstrated, in experimentally 
produced flutter, the continuous propagation of a contrac¬ 
tion wave round and round the ring of tissue surrounding 
the junction of the vena? cava? with the right auricle. This 
confirms the suggestion of Mines, 7 that circus motion could 
occur in the human heart. Mines cut a ring of tissue from 
the auricle of a large ray fish and demonstrated the phe¬ 
nomenon of circus motion thereon. He writes, “In such 
a preparation, a single stimulus, applied to any point in the 
ring, starts a wave in each direction. The waves meet on 
the opposite side of the ring and die out. But by the 
application of several stimuli in succession, it is sometimes 
possible to start a wave in one direction while the tissue on 
the other side of the point stimulated is still refractory. 
Such a wave runs round the ring sufficiently slowly for the 
refractory phase to have passed off in each part of the ring 

8 Lewis, Feil, and Stroud: Heart, 1920, vii. The observations have been ex¬ 

tensively amplified by Lewis and co-workers in a series of papers in Heart, 

viii, 1921. 

7 Mines, G. A.: Jour. Physiol., xlvi: 349, 1913. 




200 MODERN CONCEPTION OF HEART DISEASE 


when the wave approaches it. Thus, the wave circulates 
and may continue to do so for fifty revolutions or more .” 8 
The contraction wave, circulating in this central ring, sends 
contractions centrifugally off over the auricle, just as waves 
spread from a stone thrown into a pond. The rate at which 
these impulses (steadily propagated round the anatomical 
ring mentioned above) recur is so much more frequent 
than that of the sino-auricular node, that the rapid rhythm 
of the flutter dominates the heart. 

Symptoms and Signs. —The rhythm is generally con¬ 
stant. The symptoms are palpitation and, usually, those 
of cardiac embarrassment. The onset is sudden and the 
cessation gradual, usually as a result of treatment. The 
rapid auricular contractions are sometimes faintly audible. 
The ventricle rarely beats at the rapid rate of the auricle; 
in fact, some degree of heart-block is usually present. 
Therefore, the ventricular and the pulse rates may give but 
small clue to the extreme frequency of the auricular con¬ 
tractions. An irregularity may be present due to a shift¬ 
ing from 2 to 1, 4 to 1, etc., relation between the auricular 
and ventricular rhythms. 

Diagnosis. —The use of graphic methods of examina¬ 
tion, and more especially the electrocardiogram, are essen¬ 
tial to an accurate diagnosis of flutter of the auricles . 9 
Paroxysmal tachycardia differs in that it does not tend 
to the permanency that is a feature of flutter. The abrupt 
ending, and the response to vagus stimulation, so often 
noted in paroxysmal tachycardia, are not characteristic of 

8 Mines, G. A.: Jour. Physiol., xlvi: 349, 1913. 

9 Lewis, Thomas: The Mechanism and Graphic Registration of the Heart 
Beat, Paul B. Hoeber, New York, 1920. 



THE ARRHYTHMIAS 


207 


auricular flutter. The pulse is always regular in parox¬ 
ysmal tachycardia, but not necessarily so in flutter. 

Simple heart-block may be in question when the ventric¬ 
ular rate is irregular. Success in auscultating the auricular 
heart sound may disclose if the frequency of the systoles 
of the auricle is consistent with the rhythm of flutter, or 
of the slower mechanism that obtains in uncomplicated 
heart-block. With care, conclusions may, in some in¬ 
stances, be drawn from observation of the jugular pulse. 
The employment of the graphic methods will settle 
the doubt. 

Prognosis. —Flutter of the auricles has been known to 
persist for six years ; 10 it may be transient. It commonly 
is indicative of serious impairment of the heart, and the 
expectation of life is shortened. 

Treatment. —This consists in the administration of 
digitalis to the point of increasing the grade of heart-block, 
some degree of which is usually present, and in many cases 
the auricular flutter w r ill change into that of auricular 
fibrillation, and then on stopping the digitalis, normal 
rhythm will follow. This latter happy event, unfortu¬ 
nately, does not always ensue, but in these cases the digi¬ 
talis therapy is of value in that, by its power to increase 
the grade of heart-block, the ventricular rate may be kept 
down and cardiac failure averted. Quinidine sulphate (see 
chapter on treatment) will probably become a useful drug 
in the treatment of flutter. Rest in bed, and the adminis¬ 
tration of diuretics, if edema is present, are, of course, 
indicated. 


“Lewis, Feil, and Stroud: Heart , vii, 1920. 




208 MODERN CONCEPTION OF HEART DISEASE 


AURICULAR FIBRILLATION 

Auricular fibrillation has been defined by Lewis as, 
“A condition of the auricle in which some part of its muscle 
is constantly contracting, but in which the movement as a 
whole is more or less incoordinate, and therefore ineffec- 
tual .” 11 It is a frequent and important cause of irregular 
heart action. 

Etiology. —Fibrillation of the auricles may occur in 
early life and in old age, but it is most common after the 
age of twenty to twenty-five. It is stated that 25 to 50 
per cent, of the cases of fibrillation occur in patients with 
mitral stenosis, i.e., rheumatic heart disease, and after forty- 
five to fifty years of age, there appears another large wave 
of fibrillation cases in those affected with arteriosclerosis. 

Many victims of hyperthyroidism, who have been 
untreated, or in whom treatment has been unsuccessful, are 
affected later on by fibrillation. This type of arrhythmia 
may occur in pneumonia. It has been reported in diph¬ 
theria, and in syphilis. The frequency of its incidence in 
syphilis is uncertain, but it seems clear that the impression 
that fibrillation does not occur in the luetic heart is errone¬ 
ous; the writer has observed fibrillation in undoubted 
syphilitic hearts, and its association has been reported in 
the literature. On this point it seems fair to state that in 
many instances the spirochetal causation of heart disease 
is frequently unrecognized. 

Fibrillation has been produced experimentally by the 
intravenous injection of poisons, notable amongst which 
are chloroform, digitalis, strophanthin, adrenalin, nicotine, 
potassium salts, barium chloride, and aconitine. 

u Lewis, Thomas: The Mechanism and Graphic Registration of the Heart 
Beat, Paul B. Hoeber, New York, 1920. 




THE ARRHYTHMIAS 


209 


The mechanism of auricular fibrillation is closely 
related to that already described for auricular flutter, 
namely, circus movement. Lewis and his co-workers 12 
have proven that fibrillation results from circus movement, 
but the contraction wave pursues a sinuous path, both in 
outlying parts of the auricle, and in the path of the central 
wave in the ring round the junction of the vena3 cavie with 
the heart. The sinuous course of the wave is due to the 
fact that it is traveling in muscle that has not fully recov¬ 
ered from the previous contraction and is still par¬ 
tially refractory. 

Every contraction of the auricle sends a stimulus to 
contract down to the bundle of His and thence to the ven¬ 
tricle, and in accordance with this physiological fact it can 
be seen that in auricular fibrillation, in which some part 
of the auricle is almost constantly contracting, the auriculo- 
ventricular conduction tissues are being bombarded by a 
shower of impulses. Many of these may be conducted 
to the ventricle, and the latter contracts in response to as 
many as it is able. Since these stimuli vary in their 
strength and time of arrival, the rhythm of the ventricle is 
very irregular. The irregularity in the time of the ventric¬ 
ular contractions accounts directly for the variation in the 
amount of the content of the blood which can be expelled 
with each systole. Thus, many contractions may occur so 
early that the ventricle has not had sufficient time to fill 
properly, and the ventricular output may be too small to 
send a wave into the peripheral arteries or even to open 
the semilunar valves. From this it can be seen that fibrilla- 

ia Lewis, Feil, and Stboud: Heart , vii, 1920. 


14 




210 MODERN CONCEPTION OF HEART DISEASE 

tion of the auricles produces an inefficient rhythm of 
the heart. 

Pathology. —The type of lesion found varies, but 
scattered foci of inflammation and degeneration are often 
present in the auricular tissues, and most marked in the 
specialized tissues. Other pathology consistent with the 
associated heart disease, as rheumatic or arteriosclerotic 
lesions, may also be present. 

Symptoms and Signs. —In brief, these are an irregular 
rhythm of the heart, and some degree of cardiac failure. 
The irregularity is termed absolute arrhythmia, which is 
helpful in emphasizing a difference of fibrillation from all 
other cardiac arrhythmias. A rule that is rarely broken 
is that if the heart rate is 120 or more and the rhythm is 
irregular, one is almost certainly dealing with a case of 
auricular fibrillation. Exercise tends to increase the 
irregularity, which again is a distinguishing point. 

The pulse varies in volume and in rate. In patients 
resting quietly in bed, the heart rate may not be more than 
moderately elevated. If the rate is elevated, it is common 
to find that not all the beats heard by auscultation of the 
heart are represented at the wrist. The numerical differ¬ 
ence between the rate recorded at the apex and at the wrist 
is often termed “pulse deficit.” Some writers prefer to 
label “abortive” those heart beats which fail to reach the 
peripheral arteries. Unlike extrasystoles, the pause fol¬ 
lowing the heart beats which are heard obviously earlier 
than the average of their fellows bears no relation to the 
prematurity of the individual beat. 

The ventricular type of jugular pulse is present and is 
often helpful in diagnosis. When the heart rate is rapid, 


THE ARRHYTHMIAS 


211 


it is usually difficult or impossible for the observer to ana¬ 
lyze the rapid succession of waves, but in most cases there 
are occasional pauses of sufficient length to permit the 
disappearance of all waves in the cervical veins. Then 
attention should be directed to noting if the succeeding 
heart sound, heard through the stethoscope over the apex, 
is preceded by a wave in the jugular vein. This will be 
the “A” wave, described under the polygram, and it does 
not occur in auricular fibrillation. This observation may 
be assisted if care is taken that the patient is reclining at 
an angle that permits the maximum pulsation in the cer¬ 
vical veins. The observer should endeavor to see the 
silhouette of the pulsating right jugular against the back¬ 
ground of the pillow or of a dark cloth. The eye may be 
aided by placing the edge of a card, or suitable substitute, 
parallel to the vein and then observing the alteration in 
the slit between them. Too much should not be expected 
of the above visual analysis of the venous pulse on the 
first attempt, but the writer believes it will often be found 
of value if practised sufficiently to be well done, and if 
occasionally checked up by the polygram or electro¬ 
cardiogram. 

Diagnosis. —The presence of an absolute type of 
arrhythmia, usually associated with some degree of heart 
failure, is the most valuable clinical sign. Irregularity of 
the heart rhythm at the rate of 120 or more, or an increase 
of the arrhythmia following acceleration of a lower rate, 
by exercise, save for rare exceptions, indicates the presence 
of fibrillation of the auricles. The detection, by inspection, 
of the ventricular form of venous pulse, provided the ob¬ 
server is satisfied with the accuracy of his visual analysis 


212 MODERN CONCEPTION OF HEART DISEASE 


of the jugular pulse waves, is of confirmatory value. By 
the use of graphic methods, the diagnosis is easy and certain. 

Premature beats of frequent occurrence at times may 
simulate closely the arrhythmia of fibrillation. The differ¬ 
ential diagnosis has been discussed under premature beats. 

Prognosis. —Fibrillation is usually permanent, but 
may be transient. If at all persistent it is reasonable to 
presume important damage to the myocardium. Much 
improvement may result from the presence of heart-block 
produced by drug therapy, or, as sometimes happens, 
resulting from natural causes. Then the efficiency of the 
heart depends in large measure upon the integrity of the 
ventricular muscle. In other words, if the fibrillation is 
controlled by efficient treatment, the results are often very 
gratifying, but the latter must not be expected if the ven¬ 
tricular muscle is much impaired. 

Treatment. —The first principle in the treatment of 
auricular fibrillation is to administer digitalis to the point 
of inducing sufficient heart-block to prevent some of the 
shower of impulses, coming down from the auricle, from 
reaching their destination. By so doing, the ventricle is 
allowed more rest, and has time to fill properly before 
contracting. Sometimes heart-block occurs from natural 
causes, and then the patient is more comfortable, even if 
taking no medicine. 

A case of auricular fibrillation is often one of the most 
satisfying of heart conditions to treat. The removal of 
the pulse deficit in toto, or in large part, indicates that the 
correct amount of digitalization is present. The optimum 
ventricular rate varies from about 60 to 80 per minute. 
Usually the digitalis should be crowded at first, and, after 


THE ARRHYTHMIAS 


213 


digitalization has been achieved, the result may be main¬ 
tained by a suitable smaller dose. It seems fair to state 
that the patient is not receiving that to which he is entitled 
unless the drug is pushed to the point of lowering the ven¬ 
tricular rate, with the removal of all or most of the pulse 
deficit, and the marked clinical improvement, or until the 
onset of symptoms or signs of digitalis poisoning. 

The treatment of auricular fibrillation by the admin¬ 
istration of quinidine sulphate, by which, in successful cases, 
the normal rhythm is reestablished, is as yet in the experi¬ 
mental stage. The prospect is good of a real advance in 
cardiac therapy. Quinidine will be further discussed in 
the chapter on treatment. 

In conclusion, it must not be forgotten that the under¬ 
lying disease of the heart should receive adequate attention. 

HEART-BLOCK 

In this condition the essential feature is defective con¬ 
duction between the auricle and the ventricle. 

Etiology. —Heart-block has been produced experi¬ 
mentally by various procedures that interfere with the 
bundle of fibres conducting between the auricles and ven¬ 
tricles. It may result from stimulation of the vagus nerve. 
Many poisons may impair the conduction. Prominent 
among these are: digitalis, strophanthin, aconitine, mus¬ 
carine, physostigmine, nicotine, potassium salts, morphine, 
and adrenalin. The action of the latter two is by way of 
the vagus nerve, 13 while many of the others act directly 
on the conduction tissues. Heart-block occurs in asphyxia, 
anaphylaxis, and diphtheria. The most common causes in 

13 Lewis, Thomas: The Mechanism and Graphic Registration of the Heart 
Beat, Paul B. Hoeber, New York, 1920. 




214 MODERN CONCEPTION OF HEART DISEASE 


clinical cases are syphilis, arteriosclerosis, rheumatic heart 
disease, and as a result of the administration of digitalis. 

Pathology. —The findings are inconstant. Partial to 
complete destruction of the fibres of the bundle of His may 
be found. In some cases, the destruction of part of the 
fibres may so delay the conduction of impulse from the 
upper part of the heart, that the ventricle may contract in 
response to stimuli orginating in its own tissues below the 
lesion. Thus it is possible to have complete heart-block 
in life, although at autopsy the bundle is not completely 
destroyed. Of course, if the conduction defect is due solely 
to vagus action, or to the administration of digitalis, the 
condition cannot be recognized by the pathologist. In 
disease the lesions are rarely limited to the specialized tis¬ 
sues, but other parts of the heart are also involved, show¬ 
ing the changes of syphilis, rheumatic infection, arterio¬ 
sclerosis, or whatever affection may be responsible for the 
heart-block. 

Symptoms and Signs. —Some degree of heart failure 
is usually present, though some patients, whose life is not 
too strenuous, may be remarkably comfortable. 

On the other hand, grave symptoms, referable to the 
nervous system, are not uncommon. In such cases, a 
marked slowing or standstill of the ventricle produces an 
insufficiency in the supply of blood to the higher nervous 
centres, and the symptoms of cerebral anaemia result. 
These symptoms, depending on the length of the attack, 
are: pallor, transient giddiness or dimness of vision, mo¬ 
mentary loss of consciousness, convulsions, and, in the end, 
death. According to Lewis, 13 if the standstill of the ven¬ 
tricle lasts but two or three seconds, there is little disturb- 


THE ARRHYTHMIAS 


215 


ance. If the pause is for three to five seconds, a momentary 
loss of consciousness occurs. If the ventricle fails to beat 
for a longer period, as from fifteen to twenty seconds, 
twitchings or convulsive movements appear, the breathing 
deepens and becomes sighing, and cyanosis gradually 
develops. If the heart heat is in abeyance for ninety 
to one hundred and twenty seconds recovery is rarely 
witnessed. 

When complete heart-block is present, the pulse and 
ventricular rhythm are regular and of a rate averaging 
30 to 40 per minute. Higher and lower rates occur. Dur¬ 
ing the diastoles, the auricular contractions may sometimes 
be heard as faint short sounds. Inspection of the jugular 
pulse may disclose waves during the long pauses. Since 
the ventricles are then in diastole, these waves must be due 
to contractions of the auricle: they can only be confused 
with the “h” or “b” wave, which is a single wave occurring 
in early diastole, at about the time of the third heart sound. 
When the auricular systole coincides with that of the ven¬ 
tricle, careful auscultation may note a slight accentuation 
of the heart sound. 

In incomplete heart-block, the pulse may be irregular 
due to gaps caused by dropped beats. During these 
pauses, auscultation of the heart discloses a silent period, 
or, in some instances, the faint auricular sound may be 
audible. In other cases, there may be no dropped beats 
and the only suggestion of partial heart-block may be from 
the separation of the auricular and ventricular sounds, and, 
if the former is audible, a triple or gallop rhythm may 
be noted. 

As a result of exercise, in heart-block, shortness of 


216 MODERN CONCEPTION OF HEART DISEASE 

breath tends to appear readily. If the block is complete, 
the heart rate does not increase. 

Diagnosis.—A slow, regular rhythm is strongly sug¬ 
gestive of complete heart-block. When the disturbance 
is limited to some delay in conduction, the condition may 
not be recognized unless a polygram or electrocardiogram 
is obtained. Gallop rhythm may indicate partial heart- 
block. Dropped beats are due to heart-block and, excep¬ 
tionally, due to sino-auricular block. Their differentiation 
from premature beats has been discussed under the latter 
arrhythmia. In practice, the true dropped beat is rela¬ 
tively uncommon. Its confusion with an extrasystole is 
so frequent, and the difference in prognosis and treatment 
of the two conditions is so great, that it is suggested that 
the diagnosis of dropped beat be confirmed by the use of 
graphic methods. The distinction certainly cannot be 
made by palpation of the radial pulse. 

In electrocardiography, the subcutaneous injection of 
gm. 0.002 to 0.0015 (gr. 1 / 30 to V40) of atropine sulphate 
will abolish the vagus influence on the heart and determine, 
in an electrocardiogram taken about 20 to 30 minutes later, 
what part, if any, of the heart-block is due to the action 
of the vagus nerve. 

Adams-Stohes’ syndrome, in which a slow pulse is asso¬ 
ciated with fainting attacks, is thought to have been due 
to heart-block and syncope, as described above. However, 
extreme bradycardia and the attending symptoms are not 
always due to heart-block. Frequent extrasystoles may 
retard the pulse rate (though not that of the ventricle), 
and the accidental association of epilepsy of nervous origin 


THE ARRHYTHMIAS 


217 


with such a case has been reported . 14 There are a number 
of conditions in which Adams-Stokes’ syndrome may 
appear, though there may be no impairment in the auriculo- 
ventricular conduction. 

It should be remembered that an irregularity caused by 
heart-block is a regular irregularity. The author has met 
an instance where digital pressure on the vagus in the neck 
caused a prompt change from a one to one to a two to 
one rhythm and gave a superficial resemblance to the con¬ 
trol of a paroxysm of tachycardia. 

Prognosis. —This is largely dependent upon the heart 
affection of which heart-block may be but one feature. 
Heart-block due to actual lesion of the conduction tissues 
is usually permanent, if it has already persisted more than 
perhaps a few weeks; in certain acute conditions, much im¬ 
provement may occur spontaneously with the convalescence 
of the affection, usually an infection, of which it is a 
feature. Heart-block of organic causation is always a 
serious condition; sudden death is not uncommon, and if 
the block persists, survival beyond one to three years is the 
exception. There are, it is true, cases in which the patient 
lives in comparative comfort for years. 

Transient heart-block due to vagus stimulation or to 
the effect of digitalis is, of course, in a different category. 
That due to digitalis may be produced intentionally and is 
often beneficial in controlling an arrhythmia, especially 
that of auricular fibrillation. Natural heart-block is like¬ 
wise helpful here. 

Treatment. —Treatment is primarily that of the 
underlying disease. All cases of heart-block, not clearly 

14 Lewis, Thomas: The Mechanism and Graphic Registration of the Heart 
Beat, Paul B. Hoeber, New York, 1920. 



218 MODERN CONCEPTION OF HEART DISEASE 


of other causation, and occurring in patients in the age 
limits of about twenty to sixty years, should be subjected 
to the therapeutic test for syphilis. The reasons for this 
have been emphasized under cardiovascular syphilis; per¬ 
haps the chief point is that luetic heart disease tends to 
progress, and the aim should be to prevent further impair¬ 
ment of the integrity of the heart. 

Heart-block due to poisons, or the overuse of digitalis, 
will disappear by cessation of the drug. Atropine sulphate 
gm. 0.0006 to 0.0005 (gr. ‘Am to Via,), three to four times 
daily, will lift the vagus action on the conduction tissues, 
and remove that factor in the causation of the heart-block. 
When the symptoms associated with impairment of the 
blood supply of the brain are present, the recumbent pos¬ 
ture is indicated. 

It may seem paradoxical to state at one time that heart- 
block is a serious disturbance and requires treatment, and 
in the next breath, almost, to advocate the production of 
heart-block by digitalis therapy. In explanation of this 
it should be recalled that study of the physiology of exercise 
discloses that the heart may accomplish the needed increase 
in the output of blood per minute by a greater output per 
beat, and by an acceleration of the rate, i.e., more beats 
per minute. If the presence of heart-block prevents a 
ready increase in the heart rate, it becomes apparent that a 
heart so affected will be less able to meet the physiological 
demands in exercise. Therapeutic heart-block is indicated 
to combat certain unfavorable features of undue accelera¬ 
tion of the heart rate, as described under fibrillation of the 
auricles. Heart-block is then the lesser of two evils. 


THE ARRHYTHMIAS 
PULSUS ALTERNANS 


219 


Pulsus alternans can hardly be diagnosed save by using 
instrumental means of examination. It is best demon¬ 
strated in the arterial pulse tracing, but occasionally is 
present in the electrocardiogram. It may also be detected 
in the taking of the systobc blood pressure by noting that 
the number of beats coming through under the blood-pres¬ 
sure cuff is suddenly doubled as the pressure falls about 
five or more millimetres. Certain types of extrasystoles, 
namely, the interpolated, and those causing a bigeminal 
pulse, may be confused with true alternation. The use of 
graphic records will make the differentiation. 

The exact mechanism of alternation is hypothetical 
in part; the condition is generally ascribed to a variation 
in the contractility of the ventricular muscle. The ven¬ 
tricle, as is shown in the electrocardiogram, contracts regu¬ 
larly, but there is an alternation in the amount of blood 
expelled into the aorta. 

Alternation may be found when an apparently healthy 
heart is overtaxed, especially when beating at a rapid rate, 
and also in hearts in which the muscle is seriously impaired. 
It is particularly common in association with the changes 
in hypertensive heart disease, and in the arteriosclerotic 
heart, in which it may be associated with anginoid pain. 
P. D. White 15 reported its presence in one-third of the cases 
showing any degree of heart failure, in which he obtained 
pulse tracings. 

The detection of alternation is of importance chiefly 
from its bearing on prognosis. The majority of patients 
who exhibit the phenomenon of pulsus alternans succumb 


13 White, P. D.: Amer. Jour. Med. Set., cl: 82, 1915. 



220 MODERN CONCEPTION OF HEART DISEASE 


within a few years. The writer knows of a case in which 
alternation has been present most of the time for a period 
exceeding six years. 

The treatment is that of the associated heart affection. 

4 

COMBINED ARRHYTHMIAS 

In the above description, the various functional con¬ 
ditions of the heart have been described as occurring singly, 
but in practice it is common to find two or more affecting 
an individual patient. The relationship between prema¬ 
ture beats, paroxysmal tachycardia, auricular flutter, and 
auricular fibrillation, is so close that a single patient may 
be affected with all of these four arrhythmias at various 
times. The dependence of paroxysmal tachycardia on 
premature beats has been mentioned above. The fact that 
circus motion is concerned in the true mechanism of auricu¬ 
lar flutter, and, with the addition of conduction defects, 
in that of fibrillation of the auricles, has been pointed out. 
Alternation of the pulse is often more marked following 
extrasystoles, or a paroxysm of tachycardia; in fact, alter¬ 
nation may occur in the waves during a paroxysm. Most 
any of the arrhythmias may alternate with the normal 
rhythm from the sino-auricular node. 

Some degree of heart-block is the rule when the heart 
is dominated by flutter of the auricles, and the same con¬ 
duction defect is common in cases of auricular fibrillation. 
In the latter arrhythmia, when the ventricular rate is kept 
down by heart-block of natural or digitalis causation, extra¬ 
systoles may also appear. A well-known example of this 
is the bigeminy or coupling effect following the free use 
of digitalis in the treatment of fibrillation. A moment’s 


THE ARRHYTHMIAS 


221 


reflection will make it clear, as is demonstrated by the 
electrocardiogram, that since the auricles are in the grip 
of fibrillation, the premature beats must be of ventric¬ 
ular origin. 

Further examples could be given, but space forbids. 
The interpretation of combined arrhythmias is, needless 
to say, often difficult. The elucidation of some of these 
complex problems in cardiac diagnosis is one of the most 
interesting and instructive of the contributions of the 
graphic methods to clinical medicine. 



SECTION IV 


STRUCTURAL LESIONS 




CHAPTER XVIII 
STRUCTURAL LESIONS 

It would seem that until recently there has been a ten¬ 
dency to overemphasize the structural pathology of the 
heart. As urged in the chapter on “The Classification of 
Heart Disease,” it is better to think primarily in terms of 
the type of heart disease, which expresses the etiology when 
known, and then of the functional condition and structural 
changes. Realizing, however, the limitations to the above 
idealistic conception of heart affections, the writer will 
attempt in this section to present briefly data, pertaining 
to the structural pathology, which may be of value in 
diagnosis, or which may not have been sufficiently discussed 
in the preceding chapters. Although, as emphasized by 
James Mackenzie, disease processes are rarely ever limited 
to a single layer of the heart tissues, for the purpose of 
convenience, the changes in the individual layers of the 
heart will be presented separately. 

ENDOCARDIAL LESIONS 

Acute Endocarditis, as a clinical problem, is largely 
a matter of acute rheumatic heart disease, or acute septic 
heart disease. One or more murmurs are usually audible 
on auscultation, but it is often a matter of judgment as 
to whether they signify actual changes in the valvular 
endocardium. Their persistence or disappearance after a 
sufficient period of time (after convalescence is well estab¬ 
lished), and the development or absence of other signs 
and symptoms, are the safest evidence on which to make 

15 


225 


226 MODERN CONCEPTION OF HEART DISEASE 


the decision. Acute endocarditis has been sufficiently 
described under the above infections of the heart and need 
not further detain us here. 

Chronic Endocarditis is another term for chronic 
valvular heart disease, and may be considered under the 
lesions of the respective valves. The symptoms of chronic 
valvular disease show little that is distinctive of the particu¬ 
lar valves involved. It is usually by the physical signs that 
they are distinguished. 

Aortic Regurgitation. —Insufficiency of the aortic 
valve in adults is usually syphilitic, whereas the rheumatic 
infections predominate as the cause in children. When 
present in rheumatic heart disease, it is often associated 
with mitral lesions. Insufficiency and stenosis are not nearly 
so frequently associated in the aortic valve as are these 
two conditions in the mitral valve. This seems explicable 
in part from the fact that aortic insufficiency is usually 
syphilitic, and this disease (see pathology of cardiovascular 
syphilis) rarely produces stenotic change in the orifice. 

The best sign of aortic insufficiency is a diastolic mur¬ 
mur beginning with the second sound, and of maximum 
audibility along the left sternal margin, at the third and 
fourth costal cartilages. The murmur is usually audible 
also at the second right costal cartilage, and at times along 
the left border of the heart and apex, where it is to be dis¬ 
tinguished from the diastolic of mitral origin by its earlier 
commencement, higher pitch, and more blowing quality. 
As noted in the chapter on “Methods of Examination,” 
the murmur of aortic regurgitation, in some cases, is 
detected only in case the examiner applies his ear direct 
to the chest, or uses the diaphragm end piece (Bowles) of 


STRUCTURAL LESIONS 


227 


the stethoscope with the patient in the erect or leaning- 
forward posture. The aortic second sound is usually 
weakened or absent, but may be of normal intensity. 

Cardiac enlargement develops sooner or later, if the 
regurgitation is extensive; it is in just such cases that cor 
bovinum (ox heart), the largest type of heart, is found. 
The apex impulse may be displaced downward to the sixth 
or seventh intercostal space, and to the left close to the 
anterior axillary line. To the palpating hand, the impulse 
feels forceful and sustained. On Rontgen examination, 
the cardiac outline shows enlargement downward and to the 
left, with a somewhat blunted apex, and the shadow of 
the aorta is broadened, with increased pulsation, when 
examined fluoroscopically. 

A slight amount of regurgitation through the aortic 
valve, however, may exist without any obvious enlarge¬ 
ment of the heart. 

Various Vascular Phenomena are noteworthy fea¬ 
tures in patients in whom the aortic valve is insufficient. 
They are valuable confirmatory evidence of incompetency 
of the aortic valve, but are not pathognomonic unless well 
marked, as a Corrigan pulse, and even visible capillary 
pulsation may be present in individuals with low vasomo¬ 
tor tone, in some cases of exophthalmic goitre, in neuras¬ 
thenia, in congenital heart disease with a patent ductus 
arteriosus , 1 etc. 

The water-hammer, or Corrigan pulse, is one in which 
there is a quick rise and fall, so that it is often described 
as a collapsing pulse. Its chief feature, as shown by 
blood-pressure studies, is a lowering of the diastolic level, 


1 Walker, R. W. S.: Heart, ii, 3:249, 1911. 



228 MODERN CONCEPTION OF HEART DISEASE 


while the systolic remains essentially unchanged. When 
present, a visible throbbing of the carotids and other super¬ 
ficial arteries may be observed. A slight nodding or shak¬ 
ing of the head accompanies well-marked cases. 

The capillary pulse may be seen: (1), in the systolic 
flushing of a line drawn across the forehead by the finger 
or by a blunt instrument; (2), if the end of the patient’s 
fingernail is bent to the point of just blanching the pulp 
beneath; (3), as a faint pulsation, if a glass slide be pressed 
against the mucocutaneous margin of the lower lip of the 
mouth. The last method is usually the best. 

The systolic pressure in the femoral artery is often 
considerably in excess of that in the brachial (sometimes 
100 mm. of mercury higher). In explanation of this 
Starling 2 points out that the femoral artery is more rigid 
than the brachial, and the peripheral resistance is more 
definitely localized, so that the reflected waves in the artery 
occur in so short a time after the primary wave has passed 
down, that there is a summation of the two waves, with 
the production of a higher maximum and lower minimum 
pressure than was present in the waves as started in 
the aorta. 

On auscultation of the peripheral arteries, further phe¬ 
nomena of interest may be noted. This is usually most 
successfully performed if the bell of the stethoscope is 
placed over the femoral artery in Scarpa’s triangle. 

A sharp sound, called the pistol-shot sound, may be 
detected when the end of the stethoscope is in position 
over the artery, and this gives way to a systolic murmur 
if pressure is made by the instrument on the underlying 


s Starling, E. H.: Human Physiology, 3rd edition, 1920, p. 971. 



STRUCTURAL LESIONS 


229 


vessel. As the pressure is continued, a diastolic murmur 
may appear in addition, thus giving a to-and-fro murmur. 
This diastolic murmur, termed Duroziez s sign, occurs 
only in cases showing a marked Corrigan pulse, with a low 
diastolic pressure level, and is of greater value than is the 
pistol shot as an indication of insufficiency of the aortic 
valve. Duroziez’s sign is often confused with Traube’s 
sign, which is a double sound, not murmur, heard when 
the stethoscope is placed, but not pressed, over the artery. 
It is a rare sign and present only in extreme degrees of 
the water-hammer pulse. 

Functional insufficiency of the aortic valve is rare, but 
has been confirmed at autopsy. It has also been pro¬ 
duced experimentally. 3,4 

A word should be said about the mechanism of the 
vascular changes in aortic insufficiency. Since the time 
of Corrigan, it has been generally accepted that the water- 
hammer pulse is due to the actual backward flowing of 
the blood, but, as a result of experimental work, Stewart 3 4 
concludes that this type of pulse is caused by a vasomotor 
reflex which dilates the peripheral vessels. Stewart and 
Zollinger 5 have proven that the amount of blood which 
actually regurgitates into the ventricle measures but a 
few cubic centimetres. The left ventricle, then, still re¬ 
ceives the bulk of its content of blood in the usual way, i.e., 
through the much larger aperture, the mitral valve . 
Wiggers 6 admits that there is no essential backward fl ow 

3 Thayer, W. S., and MacCallum: Amer. Jour. Med. Sci., cxxxiii: 249, 1907. 

4 Stewart, H. A.: Arch. Int. Med., 1: 102, 1908. 

6 Zollinger, F.: Arch. f. Exper. Path., 61: 193, 1909. 

« Wiggers, C. J.: Modern Aspects of the Circulation in Health and 
Disease, Lea & Febiger, 1913, p. 324. 



230 MODERN CONCEPTION OF HEART DISEASE 


of blood and suggests that such would be physically im¬ 
possible in the time allowed, since the velocity of the blood 
flow is only about three-tenths of a metre per second. The 
pulse wave, however, according to Wiggers, travels at a 
rate of six to ten metres per second, and, if the writer 
reads this physiologist correctly, the latter explains the 
Corrigan pulse as directly due to a retrograde pressure 
wave. Stewart also believes that the arterial pressure is 
exerted backward into the cavity of the left ventricle, but 
holds that this retrograde pressure excites the vasomotor 
reflex, which in turn produces the Corrigan pulse. His 
paper contains considerable data in support of this con¬ 
tention. That the cardiac output is not materially in¬ 
creased is a further observation in the experiments of 
Stewart and Zollinger. 

Aortic Stenosis. —Stenosis of the aortic valve is much 
less common than is aortic insufficiency, the latter occurring 
about ten times as frequently. Aortic stenosis is often 
diagnosed when it does not exist; aneurism, aortic dilata¬ 
tion, the anaemias, etc., may also cause a systolic murmur 
at the second right costal cartilage. Puhnonary stenosis, 
with its systolic murmur and thrill, may be differentiated 
by noting that these findings have their point of maximum 
intensity to the left of the sternum and the murmur is not 
transmitted to the neck. At best the diagnosis of aortic 
stenosis is often difficult or uncertain, but this is less unfor¬ 
tunate, since this lesion is almost always a manifestation of 
rheumatic heart disease, and other evidence of that affec¬ 
tion is generally present. Syphilis almost never causes 
obstruction of the aortic orifice. 

A rough systolic murmur, accompanied by a systolic 


STRUCTURAL LESIONS 


231 


thrill, over the aortic area and transmitted to the vessels of 
the neck, usually indicates aortic stenosis. If the pulse is 
anacrotic and plateau in type, the diagnosis obtains strong 
support, hut as insufficiency of the valve usually compli¬ 
cates, the characteristic pulse findings may not be present. 
The bisferiens pulse, in which the primary wave in the 
arteriogram has a bifurcated summit, has been attributed 
to aortic stenosis, but its value in the diagnosis of this valve 
change apparently is doubtful. The second sound is often 
v r eak or absent, but distinct exceptions occur. The heart 
is usually enlarged downward and to the left, but never to 
the advanced degree found in some cases of aortic regurgi¬ 
tation. The electrocardiogram usually shows left ventric¬ 
ular preponderance. There is nothing characteristic about 
the blood pressure. On Rontgen examination, the first 
part of the aorta does not show enlargement to the extent 
so often present in aortic insufficiency. 

Mitral Regurgitation, due to actual change in the 
valve curtains, is probably always due to rheumatic heart 
disease, or its more severe type, termed septic heart disease 
in this book. Insufficiency of this valve usually occurs in 
conjunction with some degree of stenosis, but the latter 
is often not diagnosed, due to the fact that sufficient time 
(a few months) has not elapsed for it to develop, or, in 
other cases, when present, it is not easily detected. For 
further data on organic (in the sense of actual valve 
change) mitral insufficiency, the reader is referred to the 
chapter on rheumatic heart disease. 

Mitral regurgitation due to imperfect muscular co¬ 
operation in the closure of the valve is common. It occurs 


232 MODERN CONCEPTION OF HEART DISEASE 


in most febrile diseases, at times in all of the types of heart 
disease previously described, and there is good evidence 
that a small degree of it may be present even in some hearts 
which are properly classified as normal. It may be diag¬ 
nosed from the presence of a systolic murmur at the apex, 
not accompanied by evidence of enlargement of the heart. 
In some types of heart disease, however, as in cardiovascu¬ 
lar syphilis and hypertensive heart disease, cardiac hyper¬ 
trophy may be present, and yet an apical systolic murmur 
does not signify an actual valve lesion. A history of an 
infection of the rheumatic type should imply caution in 
assessing a systolic bruit as not due to valve damage. If 
a febrile disease is present it is best to withhold decision 
until it is evident that an infection has not attacked 
the valve. 

An error in the differential diagnosis between mitral 
insufficiency of non-valvular causation, and that due to 
actual lesion of the valve flaps, providing the process 
attacking the valve is at an end, is not of serious impor¬ 
tance ; for if the damage that an infection has done is limited 
to the production of mitral insufficiency, the integrity of 
the heart is but little impaired. 

Mitral Stenosis has been sufficiently discussed under 
rheumatic heart disease. 

Tricuspid Lesions are relatively rare, and when their 
clinical diagnosis is submitted to confirmation by post¬ 
mortem examination of the heart, the results are often dis¬ 
appointing. Structural change in the cusps of the tri¬ 
cuspid valve is almost always due to rheumatic or septic 
heart disease. It rarely occurs alone, but is associated with 
lesions of the mitral valve, sometimes of both the mitral and 
aortic valves, and less frequently of the pulmonic valve in 


STRUCTURAL LESIONS 233 

addition. The murmurs are soft, faint, blowing, rarely 
rough, and usually more superficial and shorter than the 
synchronous mitral murmurs. The relatively lower pres¬ 
sure which obtains in the right side of the heart is probably 
the chief factor in influencing the quality of the murmurs. 

Tricuspid Stenosis, like mitral stenosis, produces a 
mid-diastolic murmur, with or without a presystolic phase, 
and localized over and just to the left of the lower half of 
the sternum. It must be differentiated from a widely 
transmitted diastolic of mitral stenosis, and from that of 
aortic insufficiency, which latter murmur is audible both 
in the same place and higher up on the sternum, and, what 
is more important, always begins earlier in diastole. 

Tricuspid Regurgitation, due to organic change in 
the valve, usually accompanies the stenotic change, and 
much that has been said about the latter is likewise appli¬ 
cable. Its murmur is, of course, systolic and located over 
the tricuspid area. 

There are other signs of organic lesions of the tricuspid 
valve. Enlargement of the liver is often present, but 
exceptions occur. Transverse enlargement of the heart, 
increased dulness to percussion to the right of the sternum 
(over the right auricle), and a prominence of the Rontgen 
shadow of the right auricle, occur. The liver may be 
increased in size and pulsate. If there is a prominent 
wave due to auricular contraction, Mackenzie holds it as 
possible evidence of organic tricuspid stenosis. Dilated 
cervical veins, cyanosis associated in some cases with a slight 
jaundice, polycythemia, and clubbing of the fingers, are 
found in some of the more advanced cases. 

Tricuspid regurgitation, in cases in which the valve 
curtains are normal but the valve incompetent because 


234 MODERN CONCEPTION OF HEART DISEASE 


of failure of the muscular cooperation in the closure of the 
valve, is, as in the case of the mitral valve, much more 
common. It probably occurs, to some degree, in a large 
proportion of the cases of advanced heart failure, and 
perhaps in some others. The diagnosis, as made clini¬ 
cally, is usually based on non-cardiac data, for example, 
symptoms of heart failure associated with prominent pul¬ 
sation of the cervical veins, enlarged and pulsating liver, 
and sometimes ascites. If, as is often true in these cases, 
auricular fibrillation is present, the venous pulse will be 
of the ventricular type, and the symptoms of heart failure, 
as urged by Mackenzie, 7 are due to the fibrillation. The 
heart failure is never due solely to the tricuspid regurgita¬ 
tion. It is the failure of the heart to propel the blood 
forward, and not the leakage backward of some blood, that 
counts. If the auricle is acting, there is no ventricular 
jugular pulse and then the tricuspid regurgitation is of 
little importance. 

Pulmonary Valve Lesions. —Endocarditis of the 
pulmonary valve is very rare. When present it is usually 
associated with lesions of the other cardiac valves in rheu¬ 
matic heart disease. 

Pulmonary Insufficiency gives the same signs as the 
Graham Steell murmur described under rheumatic heart 
disease. 

Pulmonary Stenosis as a result of disease after birth, 
is very rare. It is to be distinguished from the congenital 
type by the history of the case and evidence of other val¬ 
vular lesions. 

A systolic murmur at the second left interspace is not 
uncommon. It has been ascribed to dilatation of the conus 


7 Mackenzie, James: Oxford Medicine, ii:465, 1920. 



STRUCTURAL LESIONS 


235 


arteriosus. Such a murmur may occur in fever and in 
anaemia. In healthy adults, this systolic murmur may be 
present during expiration and absent in inspiration. 
Without other evidence, it in no sense indicates disease, 
but is probably due to certain conditions in the relation of 
the conus arteriosus and pulmonary artery to the over- 
lying chest wall. For further data on pulmonary stenosis, 
and systolic murmurs localized at the pulmonic area, the 
reader is referred to the chapter on congenital heart disease. 

MYOCARDIAL LESIONS 

Myocarditis, as a clinical diagnosis, has been much 
abused. In some instances it would seem reasonable to 
suppose that the user’s mind worked somewhat as follows: 
“I think there is something wrong with the heart. I can’t 
hear any murmurs so I can’t blame it on a valve lesion; 
I don’t know what the trouble is, so I guess I’ll just say 
it is myocarditis.” Thus the term myocarditis has been 
applied to cases of cardiovascular syphilis, arteriosclerosis, 
hypertensive heart disease, etc., and even to cases in which 
the heart was normal. In this sense myocarditis has, at 
times, been used as a wastebasket diagnosis. 

Myocarditis is defined in the dictionary as inflammation 
of the myocardium. Of course it occurs, and in fact it 
forms an important part of the pathologists’ descriptions 
of diseased hearts. As several times previously stated, 
Mackenzie has emphasized the involvement of the myocar¬ 
dium in practically every case in which the valvular endo¬ 
cardium was attacked. The writer wishes to do nothing 
to lessen Mackenzie’s well-placed emphasis, but believes it 
will make for clearer thinking in heart affections if the 
term myocarditis is used circumspectly, as part of a larger 


236 MODERN CONCEPTION OF HEART DISEASE 


diagnosis, perhaps, and only after the case has been care¬ 
fully studied. In most instances, such study will be 
rewarded with the finding of evidence sufficient to base a 
diagnosis of one of the conditions described in the section 
on functional conditions, or of a definite type of heart 
disease, or, less frequently, of no heart disease. In the 
preceding chapters numerous references will be found to 
the various lesions of the myocardium. 

Hypertrophy. —Much that has been written on the 
subject of cardiac hypertrophy is based upon the mechani¬ 
cal conception of changes produced by valvular lesions, 
etc., but to-day this has been largely abandoned in favor 
of that of infection. Great enlargement of the heart may 
be present in cases in which the valve lesion is insignificant. 
There is an unknown factor in the causation of hypertrophy. 

Hypertrophy and dilatation are often present in the 
same heart, and it is rarely possible to determine accurately 
the extent of either. Most of the physical signs serve to 
indicate cardiac enlargement, but not the relative part of 
hypertrophy or of dilatation. It is well known that dilata¬ 
tion is a feature of the normal physiology of exercise. 

The importance of the subject is such that it may be 
well to present some of the observations made by Lewis, * * 8 
and supplemented by Cotton, 9 on hypertrophy of the 
heart. Lewis pointed out that when the heart is inspected 
in the fresh state at autopsy, and even when the organ has 
been cut in several planes, the degree of hypertrophy of 
the muscle and its relative excess in one or the other 
chamber are but imperfectly determined. These workers, 

8 Lewis, T.: “ Observations upon Ventricular Hypertrophy, with Especial 

Reference to Predominance of One or Other.Chamber,” Heart, v: 367, July, 1914. 

8 Cotton, T. F.: Heart , vi:217, Jan., 1^7. 




STRUCTURAL LESIONS 


237 


therefore, separated by a special dissection the muscula¬ 
ture of each ventricle and weighed them separately. 

According to Lewis, the commonest type of hyper¬ 
trophy is that in which the heart is uniformly hyper¬ 
trophied. In renal disease it is the rule. And in lesions of 
the aortic valve, uniform hypertrophy is almost as frequent 
as that in which it is more marked in the left ventricle. 
In aortic cases, Cotton found instances in which the right 
ventricle was hypertrophied in excess of that in the left side 
of the heart. 

It was further shown that a visible pulsation or palpable 
thrust in the epigastrium is not a particularly valuable 
sign of hypertrophy of the right side of the heart. A 
forcible and thrusting maximum impulse, displaced down¬ 
ward and to the left, is a somewhat more reliable sign 
of left ventricular hypertrophy. 

The evidence of ventricular preponderance in the 
electrocardiogram follows the ventricular weights quite 
accurately. 10 However, in uniform hypertrophy, the elec¬ 
trocardiogram shows no preponderance. 

PERICARDIAL LESIONS 

' Acute, and chronic or adhesive pericarditis, have oeen 
discussed in part under rheumatic heart disease. 

Acute Pericarditis. —It is generally a condition 
secondary to some other disease and consequently often 
escapes diagnosis. Thus it is more often disclosed at 
autopsy than diagnosed clinically. In the majority of 
instances, pericarditis is due to the rheumatic type of infec¬ 
tion, but rarer forms occur. Thus, in pulmonary tubercu- 

10 More recently exception has been found to this. Wilson and Hermann, 
see reference nine under Ventricular Preponderance, chapter iv. 




238 MODERN CONCEPTION OF HEART DISEASE 


losis, the pericardium may show a few tubercles, or be 
entirely replaced by a thick layer of fibrous and caseous 
material. Carcinoma may invade the pericardium. An 
occasional cause is infection following a wound, such as a 
stab wound. A dry pericarditis may occur as a late com¬ 
plication of nephritis. 

Williamson 11 has shown experimentally that the peri¬ 
cardial sac can hold 100 c.c. without being stretched, but 
when 655 c.c. was exceeded, the pericardium ruptured or 
was torn off the great vessels. The fluid accumulates at 
first near the apex and below, and usually pushes the left 
lobe of the liver downward. Later, as the amount of the 
fluid increases, it accumulates over the great vessels. 
Botch's sign of obliteration of the cardiohepatic angle, as 
determined by percussion, is present only in the large effu¬ 
sions, and is not found in the Rontgen examination. 

Large effusions compress the adjacent lung so that at 
times there is an area below the left scapula over which 
dulness, increased fremitus, and bronchial breathing, 
closely simulate a pneumonic process. This is usually 
designated as Ewart's or Bamberger's sign. The findings 
may lessen if the patient can assume the knee-chest posture. 
At times the doubt as to the presence of a pleuritic effusion 
is only settled as a result of a dry tap or exploratory 
thoracentesis. 

The pericardial friction murmur or rub varies from a 
feeble grazing sound to a loud grating or creaking which 
is sometimes palpable to the hand. It is not in definite 
accord with the heart sound and is liable to vary much in 
intensity from moment to moment. On expiration or firm 
pressure with the stethoscope, the murmur is commonly 


11 Williamson, C. S.: Arch. Int. Med., 25, 2:20$, 1920. 



STRUCTURAL LESIONS 


239 


intensified. Perhaps the point of greatest assistance in 
differentiating a pericardial friction sound from an endo¬ 
cardial murmur is that the former has a distinctly super¬ 
ficial quality; it sounds as though near the ear. If a rub 
is heard only near the cardiac border it may not indicate 
pericarditis, but may be of pleural origin, i.e., the pleuro¬ 
pericardial friction sound. 

If the heart is large, its anterior surface is generally in 
contact with the chest wall, and so a pericardial rub may 
be audible even in the presence of an effusion of consid¬ 
erable size. 

Percussion dulness extends well outside the apex 
impulse, and in large effusions the latter may become 
obliterated and the heart sounds feeble. Dilatation of 
the heart and pericarditis with effusion, at times are differ¬ 
entiated with difficulty. This uncertainty may exist even 
on radiographic examination, unless the plate clearly shows 
the outline of the heart separated by a lighter area from the 
outline of the pericardium. 

Treatment is, of course, based on the underlying dis¬ 
ease. If acute, rest in bed, usually with a headrest, is 
essential. Pain should be met by an icebag to the pre- 
cordia and sufficient sedatives, usually morphin or codein. 

The effusion of rheumatic origin will usually subside 
spontaneously, but if large, and there are signs of undue 
cardiac embarrassment, resort should be made to tapping 
of the pericardial sac. The best points at which to insert 
the aspirating needle are in the fifth left (or right) inter¬ 
costal space, about an inch from the sternum. Para^ 
centesis at either of these points will avoid injuring the 
internal mammary arteries, which lie about one half inch 
from the sternum, and will not pass through the pleural 


240 MODERN CONCEPTION OF HEART DISEASE 


cavity. About equally good is Sears’ point, outside the 
nipple or midclavicular line, and inside the limit of cardiac 
dulness. Under local anaesthesia and aseptic precautions, 
the needle should be passed with care and gentleness, to 
enable one to feel the giving way of the parietal peri¬ 
cardium, and to avoid cardiac trauma. Removal of but 
a small quantity frequently provokes absorption of the 
effusion. If the fluid reforms with recurrence of symp¬ 
toms, a repetition of the paracentesis may become necessary. 

Purulent pericarditis requires surgical drainage of the 
pericardium. If done promptly and well, the prognosis is 
by no means hopeless. 

Chronic Adhesive Pericarditis has been sufficiently 
described in an earlier chapter (see rheumatic heart dis¬ 
ease) . A few cases in which symptoms were marked have 
been treated surgically. The adhesions tend to reform, 
and unless the ribs overlying the heart are removed, the 
results are problematical. Opinions differ as to the value 
of this operation. The heart muscle must, furthermore, 
be in good condition to warrant surgical interference. 

Pneumopericardium, or hydro- (or pyo-) pneumo¬ 
pericarditis, is a rare condition. It may result from gas 
formation occurring after death. In life it may be pro¬ 
duced by perforation of a viscus, abscess, pulmonary cavity, 
knife in the esophagus, etc. A large accumulation of gas 
in the vicinity of the heart may simulate the above rare 
pneumopericarditis. The treatment should be surgical if 
the condition of the patient warrants interference. 

Hemopericardium. —The exudate is tinged with blood 
in certain forms of pericarditis. A large quantity of blood 
may escape into the sac in wounds, rupture of the heart, or 
rupture of an aneurism. The prognosis is favorable only 


STRUCTURAL LESIONS 


241 


in some of the traumatic cases, an increasing number of 
which have been relieved by surgery undertaken to repair 
the often associated wound of the heart. In rupture of 
the heart or of an aneurism into the pericardium, death 
results promptly or may be delayed a few hours to possibly 
a few days. 

ANEURISM 

Aneurism is usually a manifestation of syphilis, and it 
has accordingly received some attention in the chapter on 
cardiovascular syphilis. 

An aneurism may be defined in simple terms as a sac 
formed by the dilatation of the walls of an artery, and filled 
with blood. Many terms have been employed to describe 
aneurisms according as they differ in shape, size, etc., but 
perhaps the most useful are: sacculated, fusiform, dissect¬ 
ing, true, and false. A sacculated aneurism is one in which 
the sac-like dilatation opens into the artery by an opening 
which is small compared with the size of the sac, while the 
fusiform type is merely a spindle-shaped dilatation of the 
artery. The dissecting aneurism is one in which the blood 
forces a passage between the coats of the arterial wall; in 
some instances a second opening may exist by which the 
blood may reenter the lumen of the affected artery. An 
aneurism is described as true when the wall of the sac is 
formed by one or more of the walls of the artery; while 
in contrast to this the aneurism is said to be false in case 
the walls of the vessel are broken through and the blood 
retained by the surrounding tissues. From the above, 
then, it should be clear that there is much variation in the 
shape, size, and nature of the wall surrounding the differ¬ 
ent aneurisms. 


16 


242 MODERN CONCEPTION OF HEART DISEASE 


The statement that an aneurism is usually the result of 
invasion of the arterial walls by the pale spirochete is par¬ 
ticularly true of the aorta above the level of the diaphragm. 
Its rare occurrence in other infections has been mentioned 
(see cardiovascular syphilis). Whether arteriosclerosis 
ever causes an aneurismal change, is, in the light of mod¬ 
ern pathology, problematical. Before accepting a given 
aneurism as due to arteriosclerosis, the tissues should be 
studied histologically to exclude syphilis. 

Aneurisms occurring in the peripheral arteries are be¬ 
yond the limits set in this book. 

Many aneurisms are diagnosed in life only as a result 
of Rontgen examination. Even then, one involving the 
descending thoracic aorta has escaped detection until the 
patient was examined in an oblique position. Symptoms 
may arise only as a result of pressure on adjacent struc¬ 
tures, and vary according to the nature of the latter, and 
the rapidity of growth of the aneurism. In those aneu¬ 
risms which approach the surface, and may be examined by 
palpation, the demonstration of an impulse that is clearly 
expansile may clinch the diagnosis. This may be demon¬ 
strated by placing a finger of each hand on the swelling 
and noting if they are separated with each pulsation. The 
same may be accomplished by suitably placing marks with 
a skin crayon and observing if they rhythmically separate 
and approach. A valuable sign of aneurism of the trans¬ 
verse arch of the aorta is the tracheal tug. It is best 
detected by lifting the cricoid cartilage upward between 
the thumb and forefinger, and noting if there is a down¬ 
ward movement of the larynx with systole. The erect 
posture is often essential and the head should not be thrown 


STRUCTURAL LESIONS 


243 


backward. The phenomenon is due to the pushing down 
of the left bronchus by the pulsation of the aneurism. 

Rupture of the aneurism, with fatal hemorrhage, occurs 
in about 75 per cent, of the cases. Favorite locations for 
the hemorrhage are: into the pleural cavities, the peri¬ 
cardium, the left lung, through the skin, and into the 
esophagus or trachea. Death may also result from suffo¬ 
cation, cachexia, or as a result of emboli. 

Surgical Treatment, in a limited number of cases, 
has resulted in relief of pain and prolongation of life. The 
measures resorted to are reinforcement of the aortic wall 
by wrapping a strip of fibrous tissue around it, and resec¬ 
tion of the sympathetic nerves close to the aneurism, or 
of the sympathetic trunk in the neck. Treatment by the 
introduction of gold-platinum wire and electrolysis is a 
method which has benefited some cases. Its purpose is 
to promote coagulation of the blood, and the obliteration 
of the sac, by organization of the thrombus. It is most 
likely to succeed in cases in which the aneurism is of a 
definite sacculated type. The above surgical measures, 
with the exception of the operation of dividing the cervical 
sympathetic, are dangerous procedures, and perhaps their 
greatest justification is in cases attended with severe pain. 

Medical Treatment is usually symptomatic. The 
iodides in 0.6 to 1.3 gm. (10 to 20 gr.) doses appear to 
alleviate the pain. Treatment by rest, low diet, and lim¬ 
ited fluid, over a period of months, has been advocated, in 
order to encourage healing by thrombosis. Such treat¬ 
ment has a chance of success only in cases of sacculated 
aneurism with a small neck. Active individuals will not 
tolerate this method of treatment. 


244 MODERN CONCEPTION OF HEART DISEASE 


Cardiac aneurism is a rare condition. It is most com¬ 
monly located in the wall of the left ventricle, near the 
apex. An infarct of the myocardium, or syphilis, causes 
most of the cases. When the aneurism is located in the 
interventricular septum, the conduction tissues are in¬ 
volved. Rupture into the pericardial sac may terminate 
those involving the external wall of the heart. Needless 
to say, the diagnosis is rarely made in life. 


- J 




_J 

Courtesy of Frank B. Mallory 

Plate 4. Aneurism of the wall of the left ventricle with thrombus inside, associated 
with coronary sclerosis and hypertensive heart disease. 




■s**' 









SECTION V 



CHAPTER XIX 
TREATMENT 

It is the purpose of this chapter to present some of 
the therapeutic measures which, to avoid repetition, have 
been largely omitted in the earlier part of the text. 

The most important principle in cardiac therapy is 
that the latter should be preceded by the most accurate 
and complete diagnosis of the status of the heart in ques¬ 
tion. Adherence to this rule will greatly clarify both 
prognosis and treatment. 

For purposes of convenience, the treatment of heart 
affections may be roughly grouped under a number of 
general headings. 

ETIOLOGICAL TREATMENT 

To make this the more obvious is perhaps the strongest 
argument in support of the method of presentation in this 
book of diseases of the heart. The section on “Types of 
Heart Disease,” it will be noted, is based on etiology. 

Cardiovascular syphilis requires treatment directed 
against the pale spirochete. Suitable measures have al¬ 
ready been described and need not be repeated here. 

Removal of a Focus of Infection is extremely im¬ 
portant in rheumatic heart disease. The most frequent 
location of such foci is in the tonsils or teeth, but at times 
it seems fair to incriminate some other locality, such as: 
the accessory sinuses of the nose, the female pelvis, the 
prostate, septic wounds, the intestinal tract, etc. The 
evidence seems strong that the eradication of a focus of 

247 


248 MODERN CONCEPTION OF HEART DISEASE 


infection lessens the probability of a renewal or increase 
in the infection of the heart; it is difficult not to believe, in 
addition, that the prompt treatment of such foci has a 
prophylactic value in cases in which involvement of the 
heart may not yet be manifest. In occasional patients, 
unfortunately, interference with a focus of infection may 
he followed by an increase in the disturbance of the heart. 
This possibility may be considered in the prognosis of 
tonsillectomy, or other procedure, but it should not be 
allowed to prevent attempts to eradicate foci of infection. 
Further remarks on this aspect of treatment will be found 
under rheumatic heart disease. 

Infections, however mild, should be treated with greater 
care when they occur in those affected by cardiac disease. 
It would seem that if the patient is put to bed, there is 
less danger that the infection will attack the heart. 

GENERAL TREATMENT 

Rest. —Rest in bed should be the rule in all cases in 
which fever or sufficient other evidence indicates the pres¬ 
ence of an active infection in the heart. In cases present¬ 
ing the signs and symptoms of grave heart failure, the rest 
should be as absolute as possible. This means the use of 
the bedpan, of course, and at times assistance even in 
shifting position in bed. Decision as to when the patient 
may properly be allowed up should be based upon the 
duration and severity of the acute attack, and upon the 
evidence of cardiac imj^airment. The bed treatment 
should continue one or two weeks after cessation of the 
fever, and in some instances for a distinctly longer period. 
The process of getting up should he checked by noting the 
effect on the heart rate, the presence or absence of cardiac 


TREATMENT 


249 


embarrassment, etc., and the amount of liberty should be 
increased in accordance with the tolerance of the patient 
to activity. 

Rest in bed, however, is by no means of value to each 
and every case of heart disease. Except for some purpose, 
such as special study, it certainly is an error of judgment, 
or an abuse of the patient’s trust, to order him to bed 
solely because of the presence of abnormal physical signs, 
detected in examination of the heart. The carrying out 
of treatment by rest in bed imposes so much interference 
with the patient’s affairs, that it should rarely be prescribed, 
save in the presence of infection, or definite cardiac failure; 
it should be incumbent on the one who advises bed treat¬ 
ment to show benefit therefrom. Otherwise, in addition 
to the loss of time, the result may be a loss of general 
muscular tone, and a lack of confidence of ability to attend 
to one’s daily work. 

Exercise is of late assuming a more important place 
in the treatment of heart affections. Together with the 
gain in the tone of the general musculature of the body, 
there is often noted an increase in the power of the heart 
to do its work. This is explainable, in part at least, by the 
augmentation in the blood supply of the myocardium that 
is part of the physiology of muscular exertion; if the cardiac 
tissue has been impaired by inflammatory, or other changes, 
it would seem helpful to utilize any measures which might 
insure a better flow of blood through its nutrient vessels. 
In addition, it is now realized that dilatation of the heart 
may be a purely physiological process, and thus the fear 
of this feature has been much lessened. 

In practice, the amount of exercise is to be kept well 


250 MODERN CONCEPTION OF HEART DISEASE 


within the tolerance of the individual patient. The latter 
may be encouraged to pursue whatever amount of exercise 
is pleasurable; the symptoms when this limit is exceeded 
are usually so disagreeable, that the patient will be con¬ 
strained to cease exerting himself. All forms of competi¬ 
tive exercise, and those in which there is an undue incentive 
to continue, should be forbidden. The exercise should be 
repeated daily, and preferably in the open air. Sudden, 
violent, or excessive forms of physical exertion are seldom 
wise. Thus, of the games, football and tennis are undesir¬ 
able, while golf is often excellent. Exercise, then, has 
become a valuable therapeutic measure; it is often impres¬ 
sive to note how much more efficient the circulation may 
become, following systematic physical exertion of a suit¬ 
able type. 

Massage and Passive Motions. —These have a moder¬ 
ate use in early convalescence from serious heart failure. 
As soon as the patient’s condition warrants it, active exer¬ 
cise, which is much superior, is permitted. Of course, in 
patients confined to bed over long periods, massage may 
do considerable to increase the comfort and to preserve 
muscular tone. The direction of the massage stroke on 
the limbs should be towards the trunk, in order to favor 
the venous and lymph return. 

Psychic Aspects. —As in the treatment of disease in 
general, attention should be directed towards the mental 
or psychic attitude of the patient. In cardiology there is 
the bugbear of the name “heart disease.” This term may 
well be avoided, or, if it creeps in, the physician should 
take time to make clear the wide range of heart affections, 
and the lack of wisdom in being influenced by knowledge 


TREATMENT 251 

of other patients who have been said to be afflicted with 
“heart disease.” 

The analogy of valvular heart disease to the “leaky 
valve” of a mechanical pump has been overused. The 
term “leaky valve” will be found not infrequently to be 
associated by the patient with stories of unfavorable out¬ 
come in other patients. This expression may be replaced 
to advantage, perhaps, by that of “scar.” Attention can 
be drawn to the quality of the muscle of the heart, and 
what work it is able to do. In most instances, also, the 
physician may, if the subject comes under discussion, hon¬ 
estly point out the unlikelihood of sudden death. A cheer¬ 
ful, hopeful attitude of mind on the part of the patient is 
just as desirable in cardiac as in other affections. 

A considerable part of the treatment in an ambulatory 
case requires the cooperation of the patient, and to obtain 
this it is nearly always necessary to give the patient some 
knowledge of his problem. This should be stated in simple 
language that is readily understood. Experience will 
show how much it is profitable to tell the patient; it is 
rarely wise to dwell upon the unfavorable aspects of 
heart affections. 

The environment of the patient should be considered. 
Thus, the physician should see that a suitable member of 
the family has some inkling of the patient’s condition, so 
that the avoidance of certain activities will be attributed 
to their proper cause, and not to laziness. Effort directed 
towards the detection of and removal, as far as possible, 
of unfavorable influences at home or at work, such as is 
so well done by the social service department in hospital 
cases, will pay large dividends. 


252 MODERN CONCEPTION OF HEART DISEASE 


Diet. —The principles of this are simplicity, variety, 
and moderation, especially the latter. Obese patients 
should be dieted to reduce weight, which is a handicap to 
the circulation. The undernourished patient may be 
assisted to become of normal weight; at least it should be 
ascertained that the patient is on a diet sufficient to main¬ 
tain good nutrition of the body and likewise of the heart. 
In bed patients, with marked shortness of breath, food 
that requires much chewing should be avoided. When 
edema is present, the daily intake of fluid may be reduced 
to 800 to 1000 c.c., and salt may be excluded. Dietetic 
measures are of importance in the treatment of hyper¬ 
tensive heart disease (which see). 

Bowels. —Straining at stool is undesirable in cases 
affected by grave heart failure, and is dangerous if angina 
pectoris is present. Suitable measures, which do not 
need description here, should be adopted to prevent 
the foregoing. 

Baths. —Prolonged hot baths are unwise; a tepid, or 
medium hot, bath is better. Cold baths or showers are 
suitable only for patients in relatively good condition, 
and who are accustomed to them. Cold to the skin is 
contraindicated in angina pectoris. 

Baths in which the water contains certain salts, or which 
is charged with carbonic acid, have been recommended and 
extensively used at certain health resorts, as Nauheim, etc. 
There are many other features, such as the freedom from 
business cares, hygienic mode of life, etc., which doubtless 
contribute to the benefit that many patients receive. Some 
of the strongest evidence that the advocates of these baths 
have to offer is based upon change in the percussion find- 


TREATMENT 


253 


ings, which, the writer would suggest, have distinct lim¬ 
itations as proofs of scientific value. Except at these 
health resorts, balneotherapy in heart disease has not found 
much favor. 

Dress should be suitable to avoid chilling. The limbs 
may require more protection than in normal individuals. 
On the other hand, the patient should not be burdened with 
unnecessary weight from the clothing. 

Climate. —The patient does not, as a rule, change his 
residence for climatic reasons. Patients who are much 
debilitated, and those affected with arteriosclerotic heart 
disease, or angina pectoris, do better in a moderately warm 
climate. If such patients live in a region where the winters 
are severe, they may remain indoors too much, because 
of the cold; a climate which encourages outdoor life 
is preferable. 

Altitude. —In some normal men, the heart rate has 
first been found to accelerate when an altitude of five thou¬ 
sand feet 1 was reached. It is well known that those in 
whom some cardiac defect is present are more sensitive to 
a change in altitude, but anything up to one thousand feet 
is usually well tolerated. At a moderate elevation, the 
more bracing air may have a beneficial effect, and the 
patient need not, therefore, be restricted to the sea level. 

SYMPTOMATIC TREATMENT 

Pain and Restlessness. —When these symptoms are 
present in bed-patients with grave heart failure, they 
should be relieved by the administration of an opiate, such 
as morphin or codein in sufficient amount. The pain that 

‘Schneider, E. C.: “Medical Studies in Aviation,” Amer. Med. Assn., 
Chicago, 1918, p. 20. 



254 MODERN CONCEPTION OF HEART DISEASE 


is associated with acute pericarditis may be controlled, in 
large measure, by the application of an icebag to the pre- 
cordia, care being taken that the bag is not too heavy. 
The treatment of the pain of angina pectoris has been 
described under that affection. 

In milder cases, and in ambulatory patients, the above 
symptoms may often be ignored. The moderate use of 
bromides, or a few doses of veronal, is permissible. It is 
unwise to resort to the use of narcotics except in the more 
serious cases, and these latter require restriction to bed. 

Dyspncea. —The use of extra pillow r s, or of a bed-rest, 
may serve to relieve much of the difficulty. Severe re¬ 
spiratory disturbance, due to effusion into the pericardium 
or pleural cavities, may require paracentesis, which has 
been described elsewhere. 

When the dyspnoea is severe, and is associated with 
cyanosis, distention of the cervical veins, and well-marked 
increase in the cardiac dulness to the right, i.e., when there 
is evidence of increased pressure in the large veins and 
enlargement of the right auricle, and especially when, in 
addition, the radial pulse is small and weak, venesection 
may be helpful. A large vein in the bend of the elbow 
is usually selected, and blood withdrawn until there is a 
lessening in the turgescence of the veins of the neck, and a 
decrease in the evidence of marked enlargement of the right 
chambers of the heart. The amount of blood may be 8 
to 10 ounces, or two to three times that amount. In these 
cases it may be conceded that the dilatation of the heart 
is in excess of the physiologic limits, and the venesection 
acts by removing the factor of increased venous pressure. 
The resulting hydremia, or thinning, of the blood makes 


TREATMENT 


255 


easier the propulsion of the latter through the smaller 
vessels in the periphery. The blood volume is promptly 
restored, but the hydremia persists for days to weeks. This 
factor of hydremia cannot be produced by “bloodless 
venesection,” i.e., free purgation. 

Insomnia. —This should be treated by the measures 
that are appropriate when it occurs in non-cardiac cases. 
It is highly desirable that patients suffering from marked 
heart failure obtain an adequate amount of sleep. 

Gastric Disturbance. —With relief of the heart fail¬ 
ure, there may be a lessening in gastric symptoms. If gas 
is a prominent symptom, dietetic measures, such as restric¬ 
tion of carbohydrates, may be helpful. The remedies 
suggested under angina pectoris {i.e., Hoffman’s anodyne, 
etc.), may be tried. In addition, the methods used in the 
treatment of gastric disturbance presenting in patients not 
affected by heart disease are available. Tbe relation of 
gastric symptoms to the action of digitalis will be described 
under that drug. 

Edema, when present in cardiac disease, is to be 
treated by the administration of digitalis and diuretic 
drugs, to be discussed later. Since the reason that edema 
is a feature of one cardiac case with failure, and is absent 
in another, is not quite clear, the treatment of edema must 
be somewhat empirical. Reduction in the fluid intake, and 
the exclusion of salt from the diet, are indicated, but neither 
method is suitable for long periods. In intractable edema 
of severe degree, as a last resort, drainage may be accom¬ 
plished by small incisions in the skin, or by Southey’s 
capillary tubes. These last two procedures have the draw¬ 
back that the limb must be dressed aseptically, in order 


256 MODERN CONCEPTION OF HEART DISEASE 


to prevent infection. Large blebs should be evacuated 
under aseptic conditions. For further consideration of 
the problem of persistent edema, the reader is referred to 
text-books on internal medicine. 

Cardiac Standstill. —When this has occurred sud¬ 
denly, it is sometimes possible to induce the heart to resume 
beating. In some cases of Adams-Stokes’ syndrome, the 
heart action has been restored, apparently, in response to 
a vigorous slap on the precordia. Massage of the heart is 
the procedure required in most cases. 

On cessation of the heart beats, artificial respiration 
by the usual methods should first be employed. If, after 
two to four minutes, no heart sounds can be heard, the 
abdomen should be opened by a high incision, and cardiac 
massage instituted. The operator’s hand is passed into the 
abdomen, and up under the left lobe of the diaphragm, 
through which the heart may be felt. The heart is then 
compressed against the chest wall. This is done intermit¬ 
tently, and if spontaneous beats of the heart are felt, the 
massage should be interrupted for several beats, to allow 
the contractions to establish themselves. Continuous mas¬ 
sage may cause the spontaneous contractions to cease. The 
compression of the heart is then continued for a short time 
and again interrupted. After the heart has resumed beat¬ 
ing, it is safer to use too little than too much massage. 
The hand should not be withdrawn from the abdomen until 
the heart is beating well. During all this time, artificial 
respiration must be continued. Partial inversion of the 
patient will keep the cerebral centres bathed in blood, and 
assist somewhat in the filling of the heart. 

To be successful, cardiac massage should be begun 
within five minutes of the onset of the standstill. Serious 


TREATMENT 


257 


damage to the brain and clotting of the blood in the right 
ventricle follow if the heart beats are absent much over 
fifteen minutes. 


DRUG TREATMENT 

Many drugs have been administered in the therapy of 
heart affections, and but few of them are of real value. 

Digitalis, or foxglove, is far and away the most im¬ 
portant cardiac drug, and deserves, therefore, a somewhat 
fuller discussion. 

It has been clearly established that the chief action of 
digitalis, in therapeutic dosage, is the production of a les¬ 
sening of the conduction in the bridge of tissue connecting 
the auricles and ventricles. This heart-block is brought 
about by stimulation of the vagus nerve and by a direct 
action of the drug on the fibres of the bundle of His. The 
extent to which each factor is concerned in a given case 
varies with the individual patient. 2 Digitalis causes a 
shortening of the ventricular fibres, but opinions differ as 
to whether the drug also increases the contractile power 
of the heart. Clinical observations would certainly give an 
affirmative answer, but when the matter is investigated, it 
soon becomes apparent that it is extraordinarily difficult 
to obtain proof of scientific value. The slowing of the 
ventricular rate, due to the digitalis-produced heart-block, 
may account for much of the improvement in ventric¬ 
ular output. 

The weight of recent evidence would appear to be 
against a constriction of the peripheral vessels due to digi¬ 
talis. This lessens, if it does not remove, the contraindi- 

’Cushney, A. R., Marris, H. F., and Silberberg, M. D.: Heart, iv:39, 
1912-13. 


17 



258 MODERN CONCEPTION OF HEART DISEASE 


cation to digitalis in conditions of hypertension. If edema 
is associated with cardiac failure, the use of digitalis will 
often be followed by diuresis. 

The first and most constant sign of the action of digi¬ 
talis is a depression of the T wave in the electrocardiogram. 
This appears at the same time as the beginning of a thera¬ 
peutic effect, and has been demonstrated on animals to 
occur when 25 per cent, of the minimal lethal dose has been 
administered. 

Digitalis also produces a lessening of conduction in the 
auricular tissues. When pushed, the drug may cause 
extrasystoles and finally ventricular fibrillation, with death. 
The occurrence of the extrasystoles is the explanation of 
the bigeminy or digitalis coupling; its presence is an indi¬ 
cation for immediate discontinuance of the drug, as it has 
been shown 3 experimentally in cats, that when coupling 
(also extrasystoles and the phenomenon of ventricular 
escape) appears, 70 per cent, or more of the minimal lethal 
dose has been given. 

Among the earliest of the symptoms of the toxic action 
of digitalis, is loss of appetite, then nausea and vomiting. 
That this is not due to a local action on the gastric mucosa 
is evident, since it has been demonstrated that even though 
the entire gastro-intestinal tract be removed from a cat, 
and digitalis be injected intravenously, the cat will go 
through the act of vomiting. Diarrhoea is an exceptional 
result of digitalis. 

Preparation. —It makes little difference in what form 
digitalis is administered. Provided the preparation is 
potent and a sufficient amount is given, a digitalis effect 

3 Robinson, G. C., and Wilson, F. N.: Jour. Pharm. and Exper. Therap., 

10:491, 1917-18. 



TREATMENT 


259 


may be confidently expected. A well-known author 
writes: “.... in my usage of digitalis, preparation plays no 
part, for I have long since learned that the powdered leaf 
made freshly into pills is as satisfactory a form of digitalis 
as either tincture or infusion, or, if the leaf is good, just as 
effective as digipuratum and digifolin, and far less expen¬ 
sive.” 4 It should be remembered that the tincture rapidly 
loses potency if diluted with water. 

Many American-grown digitalis leaves are as potent 
as the best of those produced in Europe. There is, how¬ 
ever, no known method of growing or selecting the leaves, 
and no pharmaceutical procedure, that will ensure a prep¬ 
aration of known and unvarying strength. The only and 
reliable method of determining the potency of a given lot 
of digitalis, is that of testing the toxicity of the latter on 
cats or frogs in the laboratory. Preparations so tested 
are said to have been “standardized,” and if reasonably 
fresh, so that much deterioration has not occurred, are so 
uniform in their potency, that their therapeutic dosage 
may be calculated quite accurately before their administra¬ 
tion. It is not possible for individual druggists to conduct 
the biological tests necessary for the standardization of 
the preparations of digitalis which they dispense. When 
using these latter unstandardized products, the physician 
may be guided by their observed effects on previous pa¬ 
tients. Consequently, it is the part of wisdom to use few 
preparations and obtain them from the same source, in 
order to predict with some degree of accuracy the 
proper dosage. 

It has been shown that when digitalis is given in suffi¬ 
cient amount, a therapeutic effect may be observed in five 

4 Christian, H. A.: Amer. Jour. Med. Sci., 157:592, May, 1919. 





260 MODERN CONCEPTION OF HEART DISEASE 


to six hours, and the maximal action in twelve to eighteen 
hours. Pardee 5 found that, in the average individual, the 
body disposes of about 22 minims of the tincture per day, 
and it is necessary to replace this if it is desired to main¬ 
tain the digitalization. In this connection it is well to 
remember that minims and drops are not the same; with 
many tinctures it takes two to three drops to equal one 
minim. It may be helpful to direct the patient to measure 
his dose in a minim graduate in preference to the drop 
method. In case it is difficult for the physician to induce 
a patient to take the larger doses, which seem indicated 
by recent experience, or if he himself is held back due to 
past habits of dosage, it is suggested that a change to a 
different preparation, such as the leaf pill, may make it 
easier to administer an increased amount. The danger of 
the cumulative action of digitalis has certainly been 
overemphasized. 

Administration. —The “Eggleston Method” of dos¬ 
age and administration has become a standard, and the 
writer cannot do better than to quote freely from Eggle¬ 
ston’s 6 summary of his method. 

It is designed for rapid digitalization by oral adminis¬ 
tration. The amount of the digitalis to be used is ex¬ 
pressed in terms of the activity of the drug, and the patient's 
body weight in pounds. The activity of the drug is deter¬ 
mined by the cat method of Hatcher, 7 the unit being the 
weight of the dry drug, in milligrams, which is required 
to kill 1 kg. of cat when a solution is injected intravenously. 
This amount is called a cat unit. High-grade specimens 

6 Pardee, H. E. B.: N. T. Med. Jour., 110, 26:1064, Dec. 27, 1919. 

'Eggleston, Cary: Jour. Amer. Med. Assn.. 74, 11: 733, March 13, 1920. 

7 Hatcher, R. A., and Brody, J. G.: Amer. Jour. Pharm., 82:360, 1910. 



TREATMENT 


261 


* 

of digitalis, when not assayed by the cat unit, may be 
regarded as having an average activity of 100 mg. to the 
cat unit. The average total amount of digitalis required 
for oral administration to man is 0.15 of one cat unit per 
pound of body weight. 

The calculation of the average total amount required 
by any given patient is accomplished as follows: The 
patient’s weight (W) is determined in pounds, the cat unit 
(C.U.) of the digitalis is determined, and one of the fol¬ 
lowing formulas is applied: 

(I) ° :U13 xW ’ = grams of powdered leaf in total amount. 

(II) AIL x ^ _ cu I)j c centimetres of tincture in total 
amount. 

tt 

(HI)lW xw.= cubic centimetres of infusion in total 
amount. 

In a patient weighing 150 pounds, and when using 
digitalis having an activity of 100 mg. to the cat unit, the 
three formulas will work out to 2.25 grams (34 grains) of 
the powdered leaf, 22.5 c.c. (o V ss) of the tincture, and 
150 c.c. (5 oz.) of the infusion. 

The remainder of Eggleston’s directions and comments 
will be quoted in full. 

“Administration of Average Calculated Total 
Amount. 

(1). When the patient has received no digitalis within 
the preceding ten days. 

a . In urgent cases.—From one-third to one-half of 
the total calculated amount is administered at the first dose. 
After an interval of six hours, from one-fifth to one-fourth 
of the total is administered. After a second six hours, from 





262 MODERN CONCEPTION OF HEART DISEASE 


one-eighth to one-sixth of the total is administered. There¬ 
after, if more digitalis is needed, about one-tenth of the 
total may be repeated every six hours until maximal digital¬ 
ization is secured. In the case of the example given above 
with the total amount being 22.5 c.c. of tincture, the first 
dose would be 7 to 11 c.c., the second from 4 to 5 c.c., the 
third from 2.5 to 3.5 c.c., and thereafter about 2 c.c. every 
six hours if required. 

b. Rapid, for non-urgent cases.—About one-fourth of 
the calculated total is to be given at each of the first two 
doses, six hours apart. Thereafter about one-tenth to one- 
eighth of the total is given every six hours. 

(2.) When the patient has been taking digitalis within 
the preceding ten days. 

Before further digitalis is prescribed, the patient is to 
be subjected to the most careful examination, including 
the use of polygraphic or electrocardiographic records if 
available, to determine whether or not there are evidences 
of digitalis action. 

a. When evidences of digitalis action are absent.— 
The procedure is the same as outlined above, except that 
the total amount of digitalis required is to be reduced to 
75 per cent, of the total calculated. Thus, in the example 
used, the total would be reduced to 17 c.c. instead of the 
calculated 22.5 c.c., and the fractions prescribed at each 
dose would be based on the former figure (17 c.c.). The 
usual one-tenth of the total every six hours may then be 
prescribed if necessary. 

b. When evidences of partial digitalization are pres¬ 
ent.—It is best not to attempt to administer more than 
one-half of the total calculated amount of digitalis, divided 


TREATMENT 


263 


equally between the first three doses. In urgent cases in 
this group, however, one may administer 75 per cent, of 
the calculated amount, preferably in three equal doses, and 
then, if digitalization is not quite complete, one-tenth of 
the total amount may he prescribed every six hours. 

Safeguards. —The appearance of one or more of the 
following criteria of adequate digitalization, or of minor 
digitalis intoxication, indicates the cessation of further 
administration, either permanently or temporarily. 

(1) Nausea or vomiting (except when due to splanch¬ 
nic congestion and present before treatment is begun). 

(2) Fall of heart rate (not pulse rate) to or below 
GO a minute. 

(3) Appearance of frequent premature contractions, 
of definite heart-block, of marked phasic arrhythmia, or 
of coupled rhythm. 

The observance of a six-hour interval between doses 
allows time for complete absorption of the preceding dose 
and the development of its full action on the heart, so that 
if the patient is examined just before the administration of 
each dose, dangerous intoxication can be absolutely pre¬ 
vented. In practice it is perfectly safe to give the first 
three doses without personally examining the patient be¬ 
fore the second and third doses, if the one nursing the 
patient is properly instructed to look for nausea, vomiting, 
or slowing of the pulse to 60 or less a minute, before giving 
the succeeding dose, and to stop administration if any of 
these phenomena appear. 

When a leaf, tincture, or infusion, the cat unit of which 
is unknown, is employed, 100 mg. may be taken as the cat 
unit; but not more than 75 per cent, of the calculated total 
amount should be given in the first three doses. 


264 MODERN CONCEPTION OF HEART DISEASE 


When the patient cannot be weighed, or when marked 
edema or general anasarca is present, the body weight 
(exclusive of edema fluid) must be estimated as closely as 
possible and the total amount of digitalis calculated as 
usual. Not more than 75 per cent, of the calculated 
amount should then be given in the first three doses.” 

Many modifications of the Eggleston method have been 
made. An easy rule to follow is that of 0.1 gram (1.5 
grains) of the leaf to every ten pounds body weight of the 
patient. For digitan (American-made digipuratum) the 
same dose holds, while it is 1 c.c. (15 mm.), just ten times 
as much, for the tincture. For a 150-pound patient the 
dose would be 1.5 grams (22.5 grains) of the powdered 
leaf, and 15 c.c. (just under o ss) for the tincture. This 
is somewhat less than the amount advised by Eggleston, 
but experience shows that it is usually efficient and less 
often produces severe vomiting. A convenient method 
is to prescribe 2 pills 8 containing 0.1 gm. (1.5 grains) of 
the powdered leaf, or 2 c.c. (30 mm.) of the tincture t.i.d. 
for two to three days, and then to maintain the effect 
by one, two, or three pills (0.1 to 0.3 gm., or 1.5 to 4.5 gr.) 
of the leaf, or 1 to 3 c.c. (15 to 45 mm.) of the tincture, 
per day. The larger dose of the initial days should be 
reduced promptly if gastric symptoms appear. In cases 
in which actual vomiting results, the drug should be sus¬ 
pended until at least twenty-four hours have elapsed from 
the cessation of toxic effects. 

It is important that the saturation with digitalis be 
maintained by the small daily dose, which is to be dimin¬ 
ished or increased according to the indications in the indi- 


8 It should be three if the pills contain .06 gm. (1 gr.) of the leaf. 



TREATMENT 


26 5 


vidual patients. By so doing, many patients may be 
enabled to continue at their work, and avoid the loss of 
time, with the damage to the health, that results from 
repeated attacks of severe heart failure. From an eco¬ 
nomic standpoint alone, this is an advance over the method 
of treating solely during the attacks. 

By use of the above methods of the rapid administra¬ 
tion of digitalis by mouth, it is rare that there is a true 
need of the introduction of the drug by another route. 
When there is special urgency, ampoules of digipuratum 
(digitan), or even the tincture of digitalis may be injected 
intramuscularly, or strophanthin may be given intrave¬ 
nously. The injections of digitan or of the tincture of 
digitalis should be given deep into the gluteal or lumbar 
muscles and the site massaged vigorously for several min¬ 
utes. If given subcutaneously, or if any of the drug 
remains unabsorbed, it causes much irritation to the tissues 
and an abscess may result. The special preparations of 
digitalis are less reliable in their potency and do not con¬ 
tain all the active principles of the drug. 9 

Strophanthus, squills,apocynum , convallaria, hellebore, 
and other less well-known drugs, are members of the digi¬ 
talis group that have had their advocates. None of them 
have any advantage over digitalis, and the results of recent 
w r ork, such as that of P. D. White and his co-workers, 
demonstrate that these preparations are quite unreliable 
as regards their potency. Apocynum in therapeutic dos¬ 
age, was attended with undue vomiting. Strophanthus is 
perhaps the best of the group. They might all with advan¬ 
tage be placed in the discard. 

9 Weiss, S., and Hatciieh, R. A.: Jour. Avier. Med. Assn., 76, 8:510, Feb. 
19, 1921. 




266 MODERN CONCEPTION OF HEART DISEASE 


Strophantiiin (Ouabain is practically the same), the 
active principle of strophanthus, is attractive in that it is 
available for intravenous injection in emergencies. It 
has the objection that its potency varies, and there is, there¬ 
fore, greater danger of a sudden excessive digitalis action. 
If used, the average dose should not exceed 0.5 mg. (yjir 
gr.) of amorphous strophanthin, and 0.25 mg. ( 2 T 0 g 1 ’-) 
of the crystalline form, and should not be repeated under 
some hours unless the patient is carefully reexamined. 
As stated above, digitalis, if properly administered, is 
nearly always preferable 

Caffein. —Occasionally this drug may slow the heart 
by action on the extracardiac nerves. In animals, heart- 
block and ventricular extrasystoles have been produced. 
It is probable that, in moderate doses, caffein improves the 
efficiency of the heart. T. S. Hart, 10 as a result of the 
observation of cases showing numerous extrasystoles, and 
of one case of a paroxysm of tachycardia after theocin, 
advises caution in the use of caffein and allied drugs in 
myocardial conditions showing a high degree of irritability. 

Adrenalin is a failure as a circulatory stimulant. Its 
chief action is that of constriction of the peripheral vessels, 
and this, of course, does not facilitate the ready circulation 
of the blood. It should be employed with caution in 
anaesthesia, especially in that of chloroform, due to the 
tendency to produce extrasystoles and ventricular fibrilla¬ 
tion 11 with fatal results. The limitation of hypersensi¬ 
tiveness to adrenalin in the diagnosis of hyperthyroidism 
has been mentioned under that affection. 

10 Abnormal Myocardial Function, The Rebman Co., New York, 1917, 
p. 263. 

11 Leyy, A. G.: Heart, v: 299, 1914. 





TREATMENT 


267 


Pituitary Extract acts on the peripheral vessels, but 
has not as yet achieved any particular place in the treat¬ 
ment of heart disease. 

The Nitrites. —The value of these, especially of nitro¬ 
glycerine and amyl nitrite, has been presented under an¬ 
gina pectoris. There is no evidence of direct action on 
the heart, but the rate may be accelerated through reflex 
action on the vagus centre in the medulla. They are in 
no sense true cardiac stimulants. 

Ammonia may slow the heart rate by reflex nervous 
influences. The effect is transient. Ammonia is used in 
conditions of collapse mainly for its stimulant action on 
the central nervous system. 

Alcohol, in small doses, causes local irritation and 
also acts reflexly on the circulation. The heart is never 
directly stimulated, but depressed, by large doses. 

Camphor is supposed to stimulate, directly, the heart 
muscle, but there is an absence of scientific evidence of 
beneficial influence. Stimulation of the centres in the 
medulla is the chief action. 

Strychnine acts directly on the nervous system and 
not directly on the heart. Spartein is neither a heart 
stimulant, nor a diuretic. Barium chloride, in small doses, 
has had its advocates, but the ready appearance of extra¬ 
systoles and ventricular fibrillation, noted by Levy, 11 
should serve to exclude this drug. Cactin has been much 
advertised as a cardiac remedy, but the condition, func¬ 
tional heart disease, for which it is recommended, does 
better without drugs (see “Effort Syndrome”). Evi¬ 
dence is lacking that cactin has any beneficial effect on 
the heart. 


268 MODERN CONCEPTION OF HEART DISEASE 


Diuretics. —Digitalis itself is a diuretic in cases in 
which edema is associated with heart failure. But cer¬ 
tain drugs of the caffein, theobromine group, are even 
more efficient for this purpose. Since they are to a certain 
extent irritant to the kidney it is good policy to administer 
them on alternate days rather than for many days in suc¬ 
cession. It cannot be told in advance just which prepara¬ 
tion will cause the diuresis, and therefore if one preparation 
is not successful, it is necessary to change to another, and 
so on until the diuresis is produced. It is not often that 
all of these preparations fail, if the edema is of cardiac 
origin. The occurrence of extrasystoles has been men¬ 
tioned above, under caffein. 

Some of the more successful of these diuretic drugs, 
and their ordinary dosage, are: caffein sodiobenzoate 0.2 
gm. (3 gr.) b.i.d., theobromin sodiosalicylate (diuretin) 
0.3 to 0.5 gm. (5 to 7.5 gr.) 4 i. d., and theophyllin sodio- 
acetate 0.3 to 0.5 gm. ( 5 to 7.5 gr.) 2 to 4 i. d. Still 
another useful preparation is theocm, a synthetic theo¬ 
phylline, the latter being obtained from tea. Theocin 
sodioacetate is used in the same dosage as the theophyl¬ 
line salt. 

Quinidine Sulphate, a preparation from cinchona 
bark, is as yet in the experimental stage, but its promise 
is so great as to warrant mention. Quinidine slows con¬ 
duction in the auricular tissue and prolongs the period in 
which the latter is refractory after a contraction. This 
is taken advantage of in the treatment of auricular fibrilla¬ 
tion and flutter, in which the action of the drug may abolish 
the circus movement (see mechanism of these two arrhyth¬ 
mias). The prolongation of the refractory phase may 


TREATMENT 


260 


enable the contraction wave in the circus to close up the 
gap, and run into the area of tissue still in a refractory 
state, following the contraction in response to the wave 
in its previous circuit. This terminates the circus move¬ 
ment, and the impulses from the sino-auricular node again 
control the heart. 

There are further effects of quinidine on the heart. 
The drug shortens the conduction between the auricle and 
ventricle by a paralyzing action on the vagus nerve, very 
much like that of atropine, and also causes a lengthening 
in the conduction by direct action on the bundle. These 
are opposing actions, the extent of each varying in dif¬ 
ferent individuals. The paralyzing effect on the vagus 
accounts for the increase in the ventricular rate that is 
noted when quinidine therapy is employed. 

The administration of quinidine in auricular fibrillation 
is proving successful in about one half the cases. Some 
of these relapse, however. The chances of success appear 
to be less if the fibrillation has been present for a long 
time and if the amount of failure of the heart is consider¬ 
able; the result appears to be uninfluenced by the sex, age, 
presence or absence of a valve lesion, or character of the 
latter, etiological type of heart disease, etc. On the return 
of normal rhythm many patients experience marked relief, 
but in some no conspicuous benefit is evident. This is 
probably explainable on the ground that though the normal 
sino-auricular rhythm has been restored, extensive impair¬ 
ment of the heart may yet be present; quinidine sulphate 
cannot, of course, remove the lesions associated with rheu¬ 
matic, syphilitic, or arteriosclerotic heart disease, etc. 

It is obvious that the two effects of the drug in 
circus movement are opposing; if the effect of delay in 


270 MODERN CONCEPTION OF HEART DISEASE 


conduction in the auricular tissue preponderates, it 
is conceivable that the crest of the advancing wave may 
not be able to overtake the wave of refractory tissue in 
front of it, and the gap remains open, thus permitting the 
circus movement to continue. Also it is common for the 
action on the A-V conduction to cause an increase in the 
ventricular rate to 120 or 130, even in successfully treated 
cases, and this may force a discontinuance of the drug, 
because of the danger that the ventricle may suddenly 
develop an attack of tachycardia. The latter has occurred 
when the ventricle responds to all of the auricular con¬ 
tractions, as these are successively slowed by the drug to 
the region of 200. In an already damaged heart, such a 
ventricular rate is highly undesirable, though, fortunately, 
the effect wears off with a few hours of the discontinuance 
of the quinidine. 

The present method of quinidine therapy is somewhat 
as follows. The heart is brought under the control of 
digitalis to relieve most of the heart failure and to offset 
some of the quinidine effects on the auriculo-ventricular 
conduction. Digitalis is omitted for a few days (about 
3 to 5), to permit any excess to be eliminated. In the 
experience of the author it is well to commence the exhibi¬ 
tion of quinidine before the ventricular rate has risen over 
90, to lessen the height, if possible, of the increase in rate 
that may likely follow treatment. First, 0.2 gm. (3 gr.) 
of quinidine sulphate is given in capsules and repeated in 
two hours. If there are no untoward symptoms, it is 
probable that the patient is not hypersensitive to the drug, 
and the next day the real treatment may be instituted. 
This consists of the administration of 0.4 gm. (6 gr.) of 
quinidine sulphate 3 to 5 times per day for 3 to 5 days. 



Courtesy of Frank B. Mallory 

Plate o. Thrombi in the auricle. Note the corrugated surface of the large thrombus. 













































w 


















TREATMENT 


271 


The drug has been given for a longer period without harm, 
hut success is far more likely to occur within the first 
three days. 

It is customary to discontinue the drug when normal 
rhythm is restored, and safety demands its prompt suspen¬ 
sion if untoward symptoms appear. The symptoms of 
the toxic action of quinidine are essentially those of the 
better-known quinine. In brief these are: ringing in the 
ears, headache, nausea, vomiting, palpitation (tachy¬ 
cardia), delirium, etc. Serious respiratory paralysis was 
observed by von Frey in the original reports 12 on quinidine 
therapy. The author has encountered a single instance 
of respiratory paralysis. It occurred at the end of the 
second day of treatment in a patient in whom signs of 
toxicity of the quinidine had not previously been detected. 
Although recovery ensued, the condition was alarming. 
The maximum effect of the drug is present about two 
hours after it has been taken, and it wears away in large 
part in twelve to eighteen hours. Patients receiving 
quinidine therapy should be in bed, and seen sufficiently 
often by the physician to avoid the continuance of the drug 
after the appearance of toxic symptoms. 

Disasters have occurred as a result of the throwing off 
of an embolus from the heart. While it is known that 
auricular thrombi are more common when fibrillation is 
present, and it seems reasonable that the restoration of 
coordinate contraction of the auricle may increase the 
chance of the discharge of an embolus, it should be clearly 
remembered that the latter event occurs in cases never given 
quinidine. However, the presence of hemiplegia, or the 

“von Frey, W.: Berlin klin. Wochenschr., 55:417, May 6, 1918, and 55:819, 
Sept. 9, 1918. 



272 MODERN CONCEPTION OF HEART DISEASE 


history of the latter, if of probable embolic origin, should 
not be disregarded in deciding upon the pros and cons of 
the use of quinidine in an individual case. 

It is emphasized that the administration of quinidine in 
auricular fibrillation has not yet passed the experimental 
stage. A confident prediction is made, however, that the 
use of the drug marks a real advance in cardiac thera¬ 
peutics. Whether quinidine should be continued in small 
doses in order to prevent the relapse of a successfully 
treated case, is yet to be established. The literature on the 
use of quinidine is growing rapidly. The reader is referred 
to two particularly informing papers . 13 

13 Drury, A. N., and Iliescu, C. C.: Brit. Med. Jour., 3170: 511, Oct. 1, 1921. 

Lewis, T., Drury, A. N., Iliescu, C. C., and Wedd, A. M.: Brit. Med. Jour., 
3170:514, Oct. 1, 1921. 



APPENDIX 

ILLUSTRATIVE CASE REPORTS 

Individual case histories often are particularly effec¬ 
tive in impressing certain points. The following case 
reports have been selected as illustrating many of the con¬ 
ditions described in the preceding chapters. It has been 
necessary to limit the number of the histories, and in most 
instances the notes will be considerably abridged. It is 
better, as Sir Walter Scott said, in the preface to one of 
his novels, that the reader should occasionally be asked to 
step across a ditch than to wade through a morass of details. 

The patients to be described were seen in the Heart 
Clinic at the Boston Dispensary, in the Boston City Hos¬ 
pital, or in consultation with private physicians. In many 
instances the means of identifying the exact origin of the 
case will be purposely omitted so that it may be permissible 
to discuss the case the more freely. The object sought is 
not, of course, adverse criticism of the work of others, but 
a frank discussion of the case. 

RHEUMATIC HEART DISEASE 

Case 1 . —Hilda C— , Boston Dispensary, No. 101,639. 
Married woman, twenty-eight years of age, housewife. 

Family History .—Three children living and well. 
Two miscarriages at six weeks in the past two years. 

Past History .—At age of thirteen, was told she had a 
leaking valve of the heart and later was informed that com¬ 
plete recovery had ensued. Denies rheumatic fever, grow¬ 
ing pains, tonsillitis and chorea. Scarlet fever one year 

18 273 


274 MODERN CONCEPTION OF HEART DISEASE 


ago. Has moderate shortness of breath whenever “run 
down.” Occasionally has excessive flowing with menses. 

Present Illness. —No symptoms. Not short of breath 
on ordinary exertion. 

Physical Examination. —Thin and poorly developed; 
general stature that of visceroptosis. Many carious teeth. 

Heart. —Impulse in the fifth space just outside left 
midclavicular line. Border of deep cardiac dulness, second 
to fifth space, is convex to left. Systolic murmur at apex 
almost masking the first sound. This murmur is trans¬ 
mitted towards base and to left axilla. No diastolic mur¬ 
mur appreciated nor elicited by exercise. Regular rhythm, 
rate eighty-two. 

Wassermann reaction twice negative. 

Rontgen mensuration of heart gave figures “which are 
within normal limits except that the measurement of the 
left auricle is a little larger in proportion than the other 
measurements. The findings suggest mitral disease.” 

Treatment. —Referred to dentist. Proper corset pre¬ 
scribed. 

Subsequent History. —No diastolic murmur detected. 
No evidence of cardiac insufficiency. Patient satisfied that 
the corset is of benefit; is leading an essentially normal life. 

Diagnosis. —Rheumatic heart disease, mitral involve¬ 
ment. 

Discussion. —The character of the murmur at the apex, 
plus the evidence of cardiac enlargement (the region of the 
left auricle) as noted by physical and Rontgen examina¬ 
tion, make it probable that this is a case of rheumatic heart 
disease. After observation repeated at intervals, my 
original opinion remains unchanged in spite of the absence 
of a definite history of a disease of the rheumatic group. 


ILLUSTRATIVE CASE REPORTS 


275 


The situation at the age of thirteen is obscure and does 
not help us much. There is no evidence that the heart 
was changed by the attack of scarlet fever one year ago. 
The stature of the patient may be a sufficient cause for 
the occasional shortness of breath. 

If nothing more happens to the patient’s heart it is 
perhaps of little practical importance whether the diagnosis 
remain as at present or be changed to “Normal heart. 
Visceroptosis.” 

Case 2. —The patient was a negro boy, sixteen years 
of age. Seen with family physician. 

Chief Complaint .—Shortness of breath for one week, 
two days pain over precordia and in shoulders. 

Family History. —Parents, three brothers, and two 
sisters are living and well. One sister died of pleurisy 
and “water round the heart;” one brother has heart disease 
following rheumatic fever and chorea. 

Past History .—No scarlet fever, chorea, measles, pneu¬ 
monia or typhoid. Mumps some years ago. 

Rheumatic fever six years ago. Was ill, off and on, for 
eight months, being in bed two to three days at a time. 
The rheumatism went from joint to joint, recalls that 
ankles were visibly swollen at times. Was told that the 
heart was damaged. Has occasional attacks of tonsillitis 
but is never confined to bed because of same. During the 
past year has been well save for feeling of malaise for day 
at a time and averaging four to five times per month. 
Attributes this to gas in atmosphere (lives near gas works). 

Present Illness .—One week ago noted considerable 
shortness of breath and has been in bed past five days. 
Had been horseback riding and is thought to have over- 


276 MODERN CONCEPTION OF HEART DISEASE 


exerted. Two days ago, severe pain appeared over heart 
and the anterior aspect of both shoulders. Cannot he 
down flat the last two days. No definite chills or sweat¬ 
ing, fever not noted. 

Before this attack, the climbing of one flight of stairs 
caused dyspnoea and moderate precordial pain for two 
minutes. Walking on street caused no symptoms. 

Physical Examination .—Sitting propped up with pil¬ 
lows, moderately orthopnoeic. Fairly well developed but 
thin. Two carious teeth, tonsils prominent, no enlarge¬ 
ment of glands in the neck. Cervical veins not engorged. 

Heart. —Diffuse impulse over the precordia and ex¬ 
tending to sixth interspace almost to anterior axillary line. 
Apex impulse is ill-defined; timing of impulse over right 
ventricle and in midepigastrium shows it to be diastolic. 
Left border cardiac dulness is convex to left. To-and-fro 
friction rub audible over sternum and along right sternal 
margin. This rub is increased by pressure of the stetho¬ 
scope and when patient assumes leaning forward posture. 
Systolic murmur maximum at apex and transmitted to base 
but not to neck. At the apex the first sound is audible with 
the systolic murmur, also the second sound, and follow¬ 
ing the latter a low-pitched, diminuendo diastolic murmur. 
Pulmonic second sound accentuated and louder than aortic 
second. Heart rate eighty-five, regular rhythm. Visible 
pulsation in eleventh and twelfth space below left scapula. 

Blood pressure 90/50. Hemoglobin 80 per cent. 

Diagnosis .—Rheumatic heart disease, active, heart fail¬ 
ure considerable, mitral stenosis and regurgitation, acute 
pericarditis. 

Discussion .—Obviously a chronic case (history, and 
presence of mitral stenosis) with an acute exacerbation. 


ILLUSTRATIVE CASE REPORTS 


277 


It is not a purely mechanical disturbance of the heart but 
an active infection, as clearly shown by the pericarditis. 
The pain was of such severity as to be hardly compatible 
with an attack of simple heart failure, but was readily 
explainable by the detection of the pericarditis. The lat¬ 
ter, however, is not always painful. The formation of 
adhesions may very likely follow this acute inflammation 
of the pericardial sac. 

The history of rheumatic heart disease in a brother 
should be noted. It brings to mind the interesting obser¬ 
vation that it is not uncommon to find this disease in more 
than one child of the same family. 

The history is incomplete as there is no note as to the 
presence or absence of the pulsus paradoxus or of pressure 
signs at the base of the left lung. The condition was clear 
enough, however, without these data. 

The case was treated as an active rheumatic infection 
and improved rapidly following the free use of sodium 
salicylate. The boy returned to school about three weeks 
later. Apparently the advice as to the desirability of 
tonsillectomy in the future has been disregarded by 
his parents. 

Case 3.—A Hebrew tailor, thirty-nine years of age. 

Chief Complaint .—“Heart trouble.” Was told a year 
ago at a hospital clinic that he should return to work, 
but every time he does so, finds he has to quit after a 
couple of days. 

Family History. —Wife, two sisters, and three brothers 
are alive and well. Wife has never been pregnant. 

Past History .—Recalls no children’s diseases save 
measles. No chest trouble. Has never been particularly 
ill. “Rheumatism,” off and on, during the past ten years; 


278 MODERN CONCEPTION OF HEART DISEASE 

has never been confined to bed with it; only symptom was 
an indefinite pain in the legs. Occasional tonsillitis of 
mild degree. Denies venereal disease. 

Present Illness .—While at work is liable to suddenly 
experience a sense of pressure in the general region of the 
left nipple, then feels as though couldn’t breathe and as if 
he would choke. Has recently been told by the physician 
of his lodge that he has serious disease of a heart valve and 
that he must be very careful about exertion, for example,— 
“he must not even lean over to pick up a match.” Has to 
walk very slowly. 

No cough, swelling of feet, or shortness of breath, save 
when excited (doesn’t exert enough to know its effect 
on breath, etc.). 

Physical Examination .—Fairly well developed and 
nourished. Tonsils large, teeth in excellent condition. 

Heart .—Impulse visible and palpable in fifth space at 
nipple line; percussion of apex corresponds. The first 
sound at the apex is sharp and modified by a systolic mur¬ 
mur, the second sound is faint and followed by a low- 
pitched diastolic murmur which is diminuendo in type. 
The systolic murmur is transmitted to the base of the 
heart and to the axilla; the diastolic is audible over only 
a small area near the maximum impulse. Action regular, 
rate eighty-two. Blood pressure 140/90. Exercise test 
well tolerated; rate returned to eighty-four two min¬ 
utes later. 

Diagnosis .—Rheumatic heart disease, chronic, mitral 
stenosis and regurgitation. 

Later History .—On a subsequent visit patient admitted 
that for twenty years he had had undue shortness of breath 
on exertion. 


ILLUSTRATIVE CASE REPORTS 


279 


He was markedly hypochondriacal and several times 
ceased work because of a sensation of pins and needles all 
over his body, and sometimes a trembling of the arms and 
legs. By dint of considerable time and effort spent in 
explaining the situation and in reassuring him, he was 
enabled to overcome his fears of impending death and to 
regain control of himself. For two years he worked 
steadily at his trade, that of a stitcher in a tailoring shop. 
He learned to drive an automobile. 

Twice at intervals of one year there was hemoptysis. 
The amount was only a few teaspoonfuls and all traces of 
blood disappeared in four or five days. There was no 
fever, and no tubercle bacilli in the sputum or other evi¬ 
dence of pulmonary tuberculosis. An electrocardiogram 
showed auricular hypertrophy (i.e., P wave notched, dura¬ 
tion 0.12 second, and 3.5 104 volt). Occasional premature 
beats noted. No preponderance. Otherwise normal. 

About two and a half years after this patient was seen 
for the first time, he reported he had suddenly become 
quite short of breath during an acute chest cold, with 
which there was much cough. The sensation of being 
choked up was attributed to the cold, but it persisted stead¬ 
ily. Examination showed the presence of absolute ar¬ 
rhythmia, rate of apex being one hundred and four, that 
at wrist ninety-six, making a deficit of eight beats per 
minute. Digitan pills were prescribed, with such benefit 
that the patient has remained at work, and has little 
interest in entering the hospital to try the effect of 
quinidine therapy. 

Discussion .—The history was essentially negative for 
the occurrence of a disease of etiological significance, un¬ 
less one is satisfied with the indefinite “rheumatism” 


28 0 MODERN CONCEPTION OF HEART DISEASE 


described by the patient. The presence of mitral stenosis, 
however, justifies the diagnosis of the rheumatic type of 
heart disease. 

Attention is drawn to the two attacks of hemoptysis. 
This is not uncommon in cases affected by mitral stenosis. 
It does not appear to have any evil prognostic significance. 

The onset of auricular fibrillation at the time of some 
illness, as a chest cold, is not unusual. The appearance of 
occasional premature beats was the only suggestion that 
auricular fibrillation was more likely to ensue. 

Undoubtedly the most important feature during the 
first part of the observation of this patient was the undue 
amount of apprehension. It cost me hours of psycho¬ 
therapeutic conversation to undo what the previous physi¬ 
cian had aided in causing by his pessimistic remarks. It 
was impressive also to note the amount of improvement in 
this patient after he had gotten to believe that his heart 
was still capable, with certain limitations, of doing its duty. 

Case 4.—Thomas M., Boston dispensary, No. 24,188. 
Twenty-three years old, electrician. 

Family History .—No heart disease. 

Past History. —Measles, whooping cough. At age of 
ten years, had chorea followed by heart trouble. Tonsil¬ 
litis occasional. Tonsillectomy ten years ago. Denies 
venereal disease. 

Present Illness .—Has been in Nose and Throat Clinic 
for treatment of a peritonsillar abscess. Referred for 
examination. 

Is short of breath for about two minutes on ascending 
one flight of stairs. Can walk on street and do daily 
work without symptoms. 

Physical Examination .—Remnants of tonsils visible. 


ILLUSTRATIVE CASE REPORTS 


281 


Visible throbbing carotids, brachials, and other of the 
larger peripheral arteries. 

Heart .—Cardiac impulse visible over a wide area in 
fifth and sixth spaces from inside nipple line nearly to 
midaxilla. Timing of cardiac impulse shows that it is 
mostly a systolic retraction. Slight systolic retraction be¬ 
low left scapula. 

At the apex there is a systolic murmur trans¬ 
mitted to axilla and base. At aortic area there is another 
systolic murmur transmitted to carotid. Second aortic 
sound replaced by a loud, blowing diastolic murmur of 
greatest intensity along left sternal margin. At the 
apex the second heart sound is just audible, and follow¬ 
ing it is a low-pitched diastolic murmur. Regular rhythm, 
rate ninety. 

Slight edema over tibiae. Blood pressure 145/40 
(fourth phase). Traube’s double sound heard over 
femoral; well-marked pistol-shot and Duroziez’s sign over 
femoral and brachial arteries. Capillary pulsation present. 

Two weeks later. Traube’s sign absent. 

Wassermann reaction negative. 

Diagnosis .—Rheumatic heart disease. Aortic regurgi¬ 
tation and mitral stenosis. 

Discussion .—Since there is evidence that the heart dis¬ 
ease started at the age of ten years and followed chorea, 
it is practically certain that we are dealing with a case of 
rheumatic heairt disease. Therefore, by all odds, the most 
likely interpretation of the apical findings is organic mitral 
stenosis and not a functional condition, i.e., the condition 
described by Austin Flint. If there had been no previous 
intimation of heart disease, great care should be used before 
cardiovascular syphilis is ruled out. 


282 MODERN CONCEPTION OF HEART DISEASE 


The systolic retraction of the cardiac impulse is prob¬ 
able evidence of hypertrophy of the right ventricle; it, too, 
favors the diagnosis of organic change in the mitral valve. 
Regurgitation through the mitral valve is also present. 
The systolic retraction under the left scapula is doubtless 
the Broadbent’s sign, and indicative of pericardial adhe¬ 
sions. The latter are common with the rheumatic type of 
heart disease and probably absent with the syphilitic. 

I should not care to diagnose aortic stenosis in this case. 
Its presence would not essentially alter the prognosis or 
treatment. In fact, though this is a case of combined 
valvular lesions, it need not necessarily be of more unfa¬ 
vorable prognosis than one in which the mitral valve alone 
is affected. 

The Traube sign in the femoral is a rare finding. 

Tonsillectomy was advised. The recent occurrence of 
a peritonsillar abscess was noted in making this decision. 

SEPTIC HEART DISEASE 

Case 5. —Married woman, thirty-six years of age, born 
in Russia, a dressmaker. 

Chief Complaint .—Pain in the left side for five days. 

Family History .—Father died of asthma at age of 
eighty-four. Mother, four brothers, and three sisters are 
all alive and well; none dead. Husband died at age of 
thirty of heart disease. 

Married at sixteen. Two miscarriages with a normal 
birth between. This child dead as the result of an accident. 

Past History .—Mumps in childhood. No history of 
rheumatic fever, tonsillitis, chorea, scarlet fever, measles, 
whooping cough, pneumonia, or influenza. 

Patient has known during the past fourteen years that 


ILLUSTRATIVE CASE REPORTS 


283 


she had heart trouble. No dyspnoea, but following exertion, 
there is a sense of weakness so marked that she can hardly 
walk. There are frequent attacks of palpitation. One 
year ago swelling of the feet and legs was present for 
several weeks. Has been a bed patient in different Boston 
hospitals several times in the past twelve months. There 
has been no cough, sputum, or hemoptysis. No other 
symptoms. Has been a patient at an out-patient heart 
clinic for several months and is using pills of digitalis 
leaf daily. 

Present Illness .—Yesterday had a definite chill, lasting 
twenty minutes. Attending physician is said to have 
stated that there was some fever. During the last four 
days there has been a more or less persistent pain in the 
lower left axilla. 

Physical Examination .—Flush on cheeks, moderate 
cyanosis of lips. Apex impulse in fifth space at the left 
midclavicular line; it is accompanied by a slight thrill, 
systolic in time. At the apex there is a crescendo murmur 
ending in a sharp first heart sound; this is followed by the 
second sound, and after a just perceptible pause, by a dia¬ 
stolic roll. The latter is diminuendo in type. Pulmonic 
second sound accentuated and louder than the second sound 
at the aortic area. The rhythm is absolutely irregular; 
heart rate is seventy-five to eighty-five. 

The record reads, “Presystolic murmur at apex ending 
in a sharp first sound.” Later entries contain repeated 
notes such as, “Heart markedly irregular. Presystolic 
murmur at apex.” The electrocardiogram showed auricu¬ 
lar fibrillation. (It is reproduced in Fig. 22, the 
lower tracing.) 


284 MODERN CONCEPTION OF HEART DISEASE 


Subsequent History .—A few days after entrance quin- 
idine therapy was instituted, but it had to be discontinued 
because of headache, increasing heart rate, and orthopnoea 
which appeared following the taking of but 0.4 gin. (6 gr.). 

This patient remained in the hospital two and a half 
months. At times there were short attacks of vomiting. 
The most marked features were progressive weakness and 
emaciation associated with an irregular temperature, rang¬ 
ing from normal to a little over 102°. The remainder of 
the physical examination remained essentially unchanged. 

Death ensued two and a half months after admission 
to the hospital. 

Diagnosis .—Septic heart disease complicating chronic 
rheumatic heart disease, mitral stenosis. 

Discussion .—The diagnosis of rheumatic heart disease 
and mitral stenosis seems evident from the character of 
the diastolic murmur at the apex. An apical murmur or 
roll of this description is pathognomonic of stenosis of the 
mitral valve, except when associated with evidence of 
aortic regurgitation. 

For completeness the previous history should include 
the presence or absence of puerperal sepsis, and there 
might be some development of the statement, “Patient 
has known during the past fourteen years that she had 
heart trouble.” 

The diagnosis of septic heart disease seems most prob¬ 
able; no other cause was found to account for the chill at 
the onset of the present illness nor for the long-continued 
fever of irregular type. It is known that a septic infection 
of the heart is often engrafted on the lesions from a previous 
inflammation, especially that of rheumatic heart disease, 


ILLUSTRATIVE CASE REPORTS 


285 


Since no blood cultures were attempted, the nature of the 
infecting organism remains in doubt. The record also 
lacks evidence of the discharge of emboli, unless the pain 
in the left side were due to a splenic infarct, but experience 
shows that this feature of septic heart disease may at times 
pass unnoticed. 

Attention is drawn to the choice of the word “presys- 
tolic” for the crescendo murmur ending in the sharp first 
sound. At no time was there doubt as to the persistence 
of auricular fibrillation, but numerous observers described 
one of the murmurs at the apex as “presystolic.” Since, 
when fibrillating, the auricles no longer exhibit a coordinate 
contraction, the latter could not, as is usually said, pro¬ 
duce the murmur termed “presystolic” in this heart. The 
murmur is pre-sound but not pre-systolic, nor is it 
auriculo-systolic. 

Case 6 . —A hotel steward, fifty-one years of age. 

Present Illness .—Sudden onset of the sensation of 
weakness twenty-one days ago. Did not have a chill. 
The next day a cough with rusty, tenacious sputum set 
in. His physician reports that the patient has had a 
typical attack of lobar pneumonia of the right upper lobe. 
Said to have been desperately ill. 

One week ago the temperature fell to normal by crisis 
and the patient was fever-free for the succeeding three 
days. Each afternoon of the past three days there has 
been a chill with severe shaking. The chill persists about 
one half an hour and is associated with a rise of temperature. 

Family History .—Wife died of apoplexy; two children 
are living and well. Otherwise unimportant. 

Past History .—General health good. No history of 


286 MODERN CONCEPTION OF HEART DISEASE 


disease of etiological significance as regards the heart. 
No precordial pain, dyspnoea, palpitation, or edema. 

Physical Examination .—Looks slightly ill. Lungs. 
Slight dulness with broncho-vesicular breathing through¬ 
out the right upper lobe; over this area there are a few 
fine rales. There is slightly diminished breathing at both 
bases with some dulness. 

Heart .—Apex impulse not seen or felt. Sounds dis¬ 
tant, regular, and not rapid. The aortic second sound is 
greater than the pulmonic second; neither is accentuated. 
No murmurs are heard. 

White blood count is 14,900. 

Subsequent History .—The temperature was normal 
for two days after the patient’s admission to the hospital 
and. the opinion was that the condition was that of a 
slowly resolving pneumonia; probably not empyema. 

Five days later. Fever of an irregular type has been 
present during the past five days. The initial rise was 
accompanied by a chill and some pain in the right side, 
but, following the voiding of a large amount of urine, the 
temperature fell to normal that night. A few white cells 
and a few red cells were found in the urine. The ques¬ 
tion of a pyelo-nephritis is raised. 

Ten days after admission. The white count is 15,000. 
There is nothing definite on physical examination or on 
X-ray of the lungs to bear out the suspicion of pus in the 
chest. Nothing abnormal found in the heart. 

Fifteen days after entrance. The signs in the lungs 
remain unchanged save that there are no rales. Possibly 
this is a beginning tuberculosis, but the height of the white 


ILLUSTRATIVE CASE REPORTS 


287 


count is against that diagnosis. Several 24 -hour speci¬ 
mens of the urine have shown no pus and the kidney appears 
to have been eliminated as a possible source of trouble. 

Twentieth day. There has been a distinct chill on each 
of the past three days. Blood smears are negative for the 
plasmodia of malaria. Two successive blood cultures have 
shown Pneumococcus, Type I. This evidence can hardly 
be neglected and makes the outlook distinctly poor. There 
is nothing in the physical examination or in repeated 
X-rays to suggest the possibility of empyema. Under 
these circumstances the focus must be in the heart. 

Twenty-third day. The irregular temperature con¬ 
tinues. Yesterday the patient complained of a sudden 
pain in the left side with some spitting of blood. This 
morning there are a few rales present low in the axilla. 
The suggestion here is that of a possible small embolus to 
the lung. Four doses of antipneumococcic serum, type 
one, have been given without noticeable improvement. 

There is a friction rub in the left axilla, with moderate 
dulness and rales. The picture is not that of further 
consolidation. The heart sounds have not changed, al¬ 
though they are still very indistinct. The patient is losing 
ground day by day. 

Thirtieth day. Last night the patient suddenly com¬ 
plained of a blurring of the vision in the left eye, which 
to-day is totally blind. In addition some thickness of 
speech has appeared. The patient is becoming irrational 
and the respiratory rate is accelerating. 

Thirty-second day. Progressive weakening and death. 

Autopsy .—There is an infarct in the lower lobe of the 


288 MODERN CONCEPTION OF HEART DISEASE 


left lung. The area comprises about one third of the lobe 
and is roughly triangular in shape. 

The pericardial sac contains thirty c.c. of fluid, in which 
flakes of fibrin are evident. 

The heart weighs 325 gms. The tricuspid orifice is 
practically occluded by a large yellowish-white, friable, 
nodular vegetation, which extends along the entire base 
of one cusp. There are several smaller B-B shot vegeta¬ 
tions on a second cusp. The larger vegetative mass is 
composed of a group of smaller nodules, the whole meas¬ 
uring about 3x3 x 1.7 cm.; it approximates the opposite 
heart wall. The right ventricle is lined with a non-adherent 
red blood clot about 0.4 cm. in thickness. There is no 
evidence of ulceration about the bases of the vegetations. 
The other valves are normal. 

Diagnosis .—Septic heart disease (Pneumococcus, Type 
I), involvement of the tricuspid valve. 

Discussion .—This case was carefully studied and it is 
interesting to note the various conditions that were sus¬ 
pected as the cause of the fever, thus, pyelo-nephritis, 
empyema, tuberculosis, and malaria. As is not unusual, 
the heart showed no changes pointing to the correct diag¬ 
nosis. The blood found in the urine is a frequent occur¬ 
rence in septic heart disease. The infarcts to the lungs 
and apparently to the brain furnished a strong clue. The 
diagnosis of septic heart disease often must be made from 
the presence of an irregular fever of unexplained origin, 
the evidence of the casting off of emboli, and confirmed, 
if possible, by the finding of the causative agent in blood 
cultures. It may happen, however, that the blood culture 
results in no growth. 


ILLUSTRATIVE CASE REPORTS 289 

CARDIOVASCULAR SYPHILIS 

Case 7. —Married man, fifty-three years, real estate 
broker, seen in consultation with family physician. 

Family History .—Wife and two sons living and well. 
Paternal grandmother and some of his mother’s relatives 
suffered from asthma. 

Past History .—Asthma began at two years and has 
been present, off and on, until fifteen years ago, when an 
operation on the nose brought relief. Pneumonia at thir¬ 
teen and again at seventeen years. At the age of twenty, 
had a chancre with skin eruption, for which internal medi¬ 
cation was taken for three years. Gonorrhea at twenty- 
seven, followed shortly by an arthritis, which confined him 
to bed for two months. No definite recurrence of the 
arthritis. Four years ago an inflammation of the eye 
appeared; this was diagnosed as syphilitic by a well- 
known eye specialist. 

Present Illness .—Gradual onset of dyspnoea on exer¬ 
tion one and a half years ago. This increased so that eight 
weeks back he consulted his family physician. Marked 
edema of the legs noted the past ten days, and for four 
days he has been forced to remain sitting in a chair because 
of dyspnoea. 

Physical Examination. —Orthopnoeic, visible pulsation 
of the carotids, face pale, with slight cyanosis of lips, 
ears and hands. 

Heart .—Impulse in fifth and sixth spaces, extending 
nearly to anterior axillary line. No thrill. By percussion 
the right border is three centimetres from midsternal line, 
and the left four centimetres outside nipple. No abnormal 
dulness at base of heart. Loud, blowing, diastolic murmur 


19 


290 MODERN CONCEPTION OF HEART DISEASE 


audible from second right costal cartilage to apex, maxi¬ 
mum along left sternal margin. A systolic murmur at 
aortic area and transmitted to neck; at apex there is a 
soft systolic murmur transmitted toward axilla and base. 
Second sound heard only at base of heart. Action regular. 
There is a slight impairment of resonance at the base of 
both lungs; with some medium rales. Pulses equal, rate 
fifty-four to sixty-four, definitely Corrigan in type. A 
faint capillary pulsation is present Considerable soft 
edema of lower legs and in posterior thighs. 

A slight improvement followed the restriction of the 
fluid intake and the free use of digitalis and diuretics, 
but death occurred ten days later. 

Diagnosis .—Cardiovascular syphilis, heart failure of 
the congestive type, aortic regurgitation. 

Discussion .—This patient was suffering from an en¬ 
larged aortic regurgitant heart with cardiac failure, but 
the diagnosis should not have rested there. The condition 
was probably an advanced stage of cardiac syphilis, and if, 
at an earlier date (the patient consulted a physician at 
the time of the eye affection, four years before), vigorous 
antisyphilitic therapy had been instituted, it is possible the 
process might have been checked before the integrity of the 
heart and aorta was seriously impaired. It is known that 
true bronchial asthma does not of itself damage the heart. 
The arthritis was probably of gonorrheal origin, and if the 
same infection had attacked the heart, it would have done 
so by producing a form of septic heart disease, which, as is 
well known, is usually fatal within a relatively short period. 
Thus, having established the presence of aortic regurgita¬ 
tion, mitral stenosis, or what not, it is an error to-day not 


ILLUSTRATIVE CASE REPORTS 


291 


to go further and endeavor to determine its etiology, a 
recognition of which may be of far greater importance. 

Case 8.—Boston City Hospital, No. 425,866. Man, 
fifty-three years. 

Family History. —Wife living and well, never preg¬ 
nant. 

Past History. —Chancre admitted thirty-five years ago; 
treatment for nine months. Has had arsphenamine and 
mercury during the past five weeks. Otherwise recalls 
no previous illness until five years ago. Has lost fifty 
pounds in last two years. 

Present Illness. —Five years ago was told he had a 
“bad heart.” Since then has had occasional spells of 
shortness of breath and has been unable to work. 

Physical Examination. —Visible pulsation of carotids 
and other peripheral arteries. 

Heart. —Impulse in sixth space, almost at midaxilla. 
Soft systolic murmur at apex with first sound. At aortic 
area a diastolic murmur replaces the second sound and is 
well transmitted to left sternal margin. Rhytlim is abso¬ 
lutely irregular. 

Blood pressure 118/0, and later 128/0. Wassermann 
reaction strongly positive. The X-ray shows an enlarged 
heart and aorta. The electrocardiogram shows auricular 
fibrillation and left ventricular preponderance. 

The auricular fibrillation was brought under control 
by digitalis and subsequently removed by the use of quini- 
dine sulphate. Normal rhythm has persisted to date 
(three months). 

Diagnosis. —Cardiovascular syphilis, auricular fibrilla¬ 
tion, aortic regurgitation. 


292 MODERN CONCEPTION OF HEART DISEASE 


Discussion .—The above is similar to case No. 7, but 
apparently of slower progression. Attention is called to 
the presence of auricular fibrillation with a syphilitic heart, 
a combination which has been doubted by some. The 
response to quinidine therapy has been most helpful. 

Case 9. —Boston City Hospital, No. 424,996. Man, 
aged fifty years. 

Family History .—Wife living and well; six children 
living and well. There have been no miscarriages. 

Past History .—Frequent sore throat of moderate se¬ 
verity; no history of other infections of rheumatic group. 
Gonorrhea at eighteen; syphilis denied. 

Present Illness .—The first symptom was dysphagia 
eighteen months ago. Palpitation, dyspnoea, and cough 
past sixteen months, during which time he has been unable 
to work. For two months has had frequent attacks of 
“smothering,” most marked at night. Swelling of legs 
past week. 

Previous entries to Hospital: June, 1920, the Wasser- 
mann reaction was negative on both blood and spinal fluid. 
The X-ray showed an enlargement of the aortic shadow 
suggesting aneurism. Diagnosis: aneurism of the aortic 
arch and aortic insufficiency. July, 1920, Wassermann 
reaction strongly positive. 

Physical Examination (early in October, 1921). Left 
pupil larger than right, both react to light and distance. 
Slight cyanosis of face. Visible and palpable pulsation in 
suprasternal notch. Marked throbbing of right carotid; 
left neither visible nor palpable. 

Heart .—Impulse in sixth space well outside nipple 
line. Supracardiac dulness at first space measures 8.5 


ILLUSTRATIVE CASE REPORTS 


293 


centimetres. There is a loud systolic murmur over the 
base of the heart and it is well transmitted to neck. Dia¬ 
stolic murmur almost replacing second sound at aortic 
area and loudest along left sternal margin. At apex there 
is a systolic murmur with the first sound. Rhythm very 
irregular, averaging twenty-five per minute. Pulse at 
right wrist is well-marked Corrigan in type; that on left is 
barely palpable. Liver, lower border palpable five centi¬ 
metres below costal margin in right mammary line, upper 
border at sixth rib. Marked edema of legs and external 
genitalia. 

Rontgen examination demonstrates a fusiform enlarge¬ 
ment of the transverse part of the aortic arch. 

The electrocardiogram showed heart-block not quite 
complete, for the ventricular rate varied from a two to one 
to a one to one rhythm with the auricle. At times the 
additional “a” waves could be distinctly seen in the venous 
pulse of the neck during cardiac diastole. 

The severe heart failure continued, and death followed 
early in October, 1921. A limited autopsy was obtained 
and disclosed a large aneurism of the transverse aortic arch, 
and this almost obliterated the openings of the left carotid 
and subclavian arteries. The aortic wall showed advanced 
syphilitic changes which were continued down to the aortic 
cusps. The heart was considerably enlarged; except for 
the fibrous thickening of the aortic valve, the valves were 
normal. Microscopic examination was not made. 

Diagnosis .—Cardiovascular syphilis, partial heart- 
block, heart failure, aortic regurgitation, and aneurism 
of the transverse part of the aortic arch. 

Discussion .—The symptoms of this aneurism began 


294 MODERN CONCEPTION OF HEART DISEASE 


eighteen months before death. The negative Wassermann 
reactions on both blood and spinal fluid in June, 1920, 
should be noted. Too many diagnoses of cardiovascular 
syphilis are discarded because of a negative Wassermann 
test. It is obvious from the description that this was an 
advanced case, and relatively hopeless to treat. 

It is noteworthy that this patient was the father of six 
apparently healthy children. Perhaps undue emphasis 
has been placed upon the association of miscarriages and 
syphilis in the parents. 

The pronounced systolic murmur at the aortic area and 
transmitted to the neck was proven not to be due to actual 
stenosis of the aortic valve. 

The diagnosis of heart-block was easily made at the 
bedside by the plainly visible waves in the jugular vein 
when the heart (ventricular) rate was slow. That the 
block was not complete could be inferred from the changing 
rate, the latter sometimes being sixty or more per minute. 

Case 10.—Boston City Hospital, No. 429,730. Single 
man, forty-six years, member of fire department. 

Chief Complaint ,—Daily attacks of pain, starting in 
right lower jaw and radiating to right neck, arms, 
and precordia. 

Family History. —Unimportant. 

Past History .—Never sick except for accidents. In 
1911, fall on spine; 1916, fracture of left tibia; 1917, frac¬ 
ture of left olecranon process; 1920, fracture of left clav¬ 
icle, right humerus, sternum, and several ribs. Denies 
venereal disease by name and by symptoms. 

Present Illness .—Since March, 1921 (eleven months 
ago), has had frequent attacks of pain which apparently 


ILLUSTRATIVE CASE REPORTS 


295 


starts in right lower molar tooth and radiates to neck, 
shoulder, and arm on the right side, and to the upper pre- 
cordia. Occasionally the pain radiates to the left shoulder 
and arm. These attacks follow exertion or the attempt 
to walk against a cold wind. The pain is severe enough 
to force the patient to discontinue whatever he is doing 
and remain motionless. Believes it would be a great effort 
to speak during the attack. The latter lasts for only 
about two to five minutes. Is conscious of a distinct les¬ 
sening of physical power since the attacks began eleven 
months ago. 

Physical Examination .—Teeth appear normal; no 
tenderness to pressure on right lower molar. 

Heart. —Increased supracardiac dulness especially to 
the right at first intercostal space. Soft systolic mur¬ 
mur at aortic area and transmitted to neck. Blood 
pressure 104/76. 

X-ray of teeth shows no pathology. The chest plates 
show a prominence of the aortic shadow to the right. 
Width of great vessels six centimetres. The cardiac apex 
is lowered into the left curve of the diaphragm, and the 
outline of the lateral wall of the left ventricle is lengthened. 
Transverse diameter of heart sixteen centimetres. 

The Wassermann reaction on two occasions was mod¬ 
erately positive. 

The electrocardiogram was normal. 

Diagnosis .—Probably cardiovascular syphilis, angina 
pectoris. 

Discussion .—A case of angina pectoris, and at the 
patient’s age, forty-six years, should first suggest syphilis 
as the cause. It is true that the point of origin of the pain 


296 MODERN CONCEPTION OF HEART DISEASE 


is atypical, but such occurs and has been described by Sir 
James Mackenzie in his book on heart disease. The asso¬ 
ciation of the pain with exertion and the other data pertain¬ 
ing to the attacks are of considerable supporting value to 
the diagnosis. The history of the numerous injuries is 
somewhat confusing, but should not, it would seem, prevent 
the diagnosis of angina pectoris, probably of luetic origin. 
The X-ray and Wassermann lend some support to this 
diagnosis. It is extremely important that a therapeutic 
test of antisyphilitic treatment be instituted without delay. 
The patient was discharged to his private physician with 
this advice. 

ARTERIOSCLEROTIC HEART DISEASE 

Case 11.—Married woman, aged seventy years. 

Complaint .—A few months ago was told by family 
physician that she had valvular heart disease and must be 
very careful about physical exertion. 

Past History .—Measles at the age of twenty-two years. 
Is positive she has had no other diseases. Health has 
been excellent, save for some pain in the feet and lower 
back, for which she has been under the care of an 
orthopedist. 

Present Illness .—A few months ago was told of the 
presence of a murmur indicating a leaky valve of the heart. 
Since then has noted that she must take her time on ascend¬ 
ing stairs. Walks considerably but is a little short of breath 
on ascending hills. At times is conscious of a slight aching 
under the right breast; this is not a real pain and is never 
felt higher up over the precordia, and there is no radiation 
to the arms or shoulders. At times the heart pounds a 


ILLUSTRATIVE CASE REPORTS 


297 


little (indicates by motion of hand a rate estimated at 
about one hundred per minute). 

Physical Examination. —A fairly well-developed wom¬ 
an, somewhat thin; looks ten years less than her stated 
age. Arcus senilis present. Some of molar teeth absent, 
remainder in excellent condition. 

Heart .—Impulse in fifth space at left midclavicular 
line. A slight systolic thrill is present. Percussion 
borders of heart normal, no increase in supracardiac dul- 
ness. Regular rhythm, rate seventy-two. Loud, rough 
systolic murmur with first sound at apex, transmitted 
toward base. A faint systolic murmur at the second right 
costal cartilage and propagated slightly toward carotid. 
No diastolic murmur heard. Light exercise well tol¬ 
erated, no essential change in heart findings. Blood 
pressure 160/95. 

Diagnosis .—Arteriosclerotic heart disease. 

Discussion .—The murmur at the apex was doubtless 
due to the regurgitation of blood through the mitral valve, 
and the latter may have undergone some of the changes 
found in arteriosclerosis, but it is doubtful if any good pur¬ 
pose would be served by adding mitral regurgitation to 
the diagnosis. It seems better to restrict this term to cases 
in which there is also evidence of cardiac enlargement and 
a history of infection of the rheumatic type. The picture 
associated with a “leaky valve” was not truly present. 

Also heart failure can hardly be said to be present, as 
this lady could do fully as much if not more than the aver¬ 
age for her age and type. The diagnosis of valvular heart 
disease was based apparently on the auscultatory findings; 
a systolic murmur without other evidence of abnormality 


298 MODERN CONCEPTION OF HEART DISEASE 

is insufficient grounds for the diagnosis of an organic 
change in the valve. The age of seventy years may be 
said to justify placing this patient in the arteriosclerotic 
group and by so doing the problems of prognosis and treat¬ 
ment are clarified. 

Case 12. —Retired business man, aged seventy-one. 

Chief Complaint .—Severe attacks of substernal pain 
past six months. 

Family History. —Unimportant. 

Past History .—Good health until recent years. Ap¬ 
pendectomy five years ago. Since then has had some lack 
of control of the bladder; told it is due to an enlarged 
prostate gland. Three years ago had pneumonia; was in 
bed two weeks. One year ago “rheumatism,” evidenced 
by pain in left upper arm. This pain was not associated 
with exertion, and was of but a few minutes’ duration at 
a time. 

Present Illness .—Six months ago, while walking hur¬ 
riedly, was seized by pain in throat (just below larynx). 
On stopping a few minutes the pain ceased. About three 
days later had a similar attack on ascending stairs. Now 
the attacks occur daily and sometimes several times per day. 

The present attacks occur mostly in the evening and 
may follow even the exertion of undressing. The chief 
pain is under the midsternum, and may radiate to either 
upper arm, the left forearm, and occasionally to both mid¬ 
dle fingers. The pain is severe enough to bring tears to 
the patient’s eyes, and when it is present he must cease 
speaking and keep motionless. During end of attack the 
patient expels considerable gas from stomach. Has been 
given one and two drop doses of nitroglycerine but has not 
noted any effect. 


ILLUSTRATIVE CASE REPORTS 


299 


Tobacco and alcohol none. No coffee for several 
months. Bowels always costive. 

Physical Examination. —Thin, nervous man, looks his 
age. Pupils equal and react to light and distance; arcus 
senilis present. Three carious teeth. 

Heart .—Supracardiac dulness four by three centi¬ 
metres, palpable pulsation in suprasternal notch. Cardiac 
impulse faintly palpable in fifth space just inside left mid- 
clavicular line; left cardiac border inside nipple line. 
Heart sounds of fair quality, the normal physiological 
difference between the first and second sound at the apex 
is lessened. At the aortic area there is a faint systolic 
murmur transmitted slightly toward the right neck. Heart 
rate eighty-two, regular rhythm. 

Knee j erks present and equal. No edema of legs. 

Blood pressure 145/90. 

Urine clear, slightly pale, specific gravity 1008, no 
albumen, no sugar. 

Rontgen examination. Heart slightly small in size. 
Prominence of aortic knob and “tortuous” appearance 
to aorta. 

Diagnosis .—Arteriosclerotic heart disease, angina 
pectoris. 

This patient obtained “wonderful relief” from the use 
of nitroglycerine (tablet of Vioo grain under the tongue) 
and a considerable lessening of the gastric flatus after tak¬ 
ing Hoffman’s anodyne (as described in Chapter XVI). 
However, he never regained much physical power. At 
times digitalis was prescribed but without marked benefit. 
The angina was promptly controlled and never returned 
with any severity. Death ensued some eighteen months 


300 MODERN CONCEPTION OF HEART DISEASE 


later, the last month being spent in bed and the picture 
being that of old age and moderate heart failure. 

Discussion .—As is not uncommon, the relief of the 
symptoms of angina pectoris was followed by abundant 
evidence that the patient’s heart was insufficient; in a word, 
he became a chronic invalid. Experience has shown that 
little else can be expected when angina pectoris appears 
in the elderly. 

The success obtained by the administration of nitro¬ 
glycerine, in spite of its failure when previously prescribed, 
should be noted. In my opinion the method and prepara¬ 
tion were less favorable. It is also suggested that the 
particular solution may have lost some of its potency, no 
effect being observed. The drug should be used in increas¬ 
ing dosage until relief or toxic symptoms result. 

HYPERTENSIVE HEART DISEASE 

Case 13. —Housewife, forty-two years of age, born in 
England. Boston Dispensary, No. 183,822. 

Family History .—Father and mother died of old age. 
One sister and one brother are alive and well. Husband 
in good health. No children, no miscarriages. 

Past History .—Measles and mumps in childhood. In¬ 
fluenza three years ago, erysipelas two years past. 

Present Illness .—For two years has had much frontal 
headache. Urination frequent at night. Gradual lessen¬ 
ing of strength. Occasional puffiness of ankles, face, and 
hands. Repeated urinary examinations have shown a spe¬ 
cific gravity of 1008 to 1012, with albumen varying from 
a slight trace to a trace. The sediment has usually been 
free of pathological elements, but rarely has shown a hyalin 
granular cast. 


ILLUSTRATIVE CASE REPORTS 301 

The Wassermann test has been negative. The blood 
examination showed hemoglobin of sixty-five per cent., 
with three million red cells. The differential count of the 
white corpuscles, and the appearance of the red cells in the 
stained smear were essentially normal. 

Has been treated by diet, etc., with indifferent success. 
Sent to Heart Clinic for consultation. 

Physical Examination .—Considerable pallor; patient 
looks sick. 

Heart .—Impulse in fifth space, almost at anterior axil¬ 
lary line. Percussion suggests enlarged heart. At the 
apex there is a loud systolic murmur with the first sound, 
and transmitted toward base and axilla. Regular rhythm, 
rate eighty-four. Blood pressure 175 / 126 . 

This patient was referred to the Massachusetts General 
Hospital, where she died eleven days later. The diagnosis 
was: chronic nephritis, uremia. 

Discussion .—It was recognized that this patient was 
losing ground in spite of almost two years of treatment as 
an outpatient. The anaemia, and the comparatively fixed 
specific gravity of the urine, with the other data, pointed to 
damage to the kidneys. The belief that a serious condi¬ 
tion was jDresent suggested the desirability of recommend¬ 
ing the patient for admission to a hospital in order that 
a more thorough investigation of the condition of the kid¬ 
neys might be made. 

Some would prefer to classify this case simply as 
chronic nephritis, but from the standpoint of cardiology it 
belongs in the group of hypertensive heart disease with 
chronic nephritis. 

Case 14 . —Male printer, aged fifty-one years. Seen 
in consultation with family physician. 


302 MODERN CONCEPTION OF HEART DISEASE 


Present Illness .—Four days ago, when first seen by 
physician, appeared to be about “all in;” was dusky, dysp- 
noeic and staggering in gait. Sent to bed at once. Has 
had no fever nor clear-cut cough, but there have been 
pulmonary signs suggesting pneumonia, and some evidence 
of heart failure. 

No pain near heart and none in arms or shoulders. 
Admits that there has been considerable shortness of breath 
for three months, following some heavy lifting. During 
the past two weeks has spent considerable time at night 
sitting in a chair, as breathing has been easier thus. 

Past History .—Two years ago the blood pressure was 
about one hundred and eighty, and has been high since 
then. Has worked hard but has enjoyed fair health. 
Further history not obtained (in part because of patient’s 
poor condition). 

Physical Examination .—Markedly orthopnoeic, slightly 
cyanotic. Chest deformed (pigeon breast, scoliosis, and 
dorsal kyphosis). Coarse moist rales in both axillae. 
Impairment of resonance at right apex from second rib in 
front to spine of scapula behind. Over this area the breath 
sounds are weakened. High up in the right axilla there 
is a broncho-vesicular respiration and some rales of a crepi¬ 
tant type (not quite the fine crepitant rales of Laennec). 

Heart .—Impulse in fifth space outside nipple line. No 
increased supracardiac dulness. Due to deformity of 
chest, it is hard to estimate the size of the heart by per¬ 
cussion, hut by comparison of its contour with the stature 
of the patient, it would appear to be enlarged. Absolute 
arrhythmia present; rate at apex one hundred and twenty- 
six, at wrist one hundred and five, pulse deficit twenty-one. 


ILLUSTRATIVE CASE REPORTS 


303 


Cervical veins engorged, no auricular wave visible on in¬ 
spection. Second sounds present at base, systolic mur¬ 
mur at apex. 

Diagnosis .—Auricular fibrillation in a heart that is 
probably hypertensive. Pulmonary condition uncertain; 
probably beginning consolidation of right upper lobe, but 
the findings may be due to the chest deformity plus the 
rales associated with severe heart failure. 

Subsequent History .—The free use of digitalis was 
followed by a satisfactory control of the auricular fibrilla¬ 
tion, the heart rate dropping to eighty to ninety with 
practically no deficit. The rales disappeared from the 
chest, but otherwise the physical signs in the right axilla 
remained unchanged. Pever remained absent and there 
was no further evidence of pneumonia. 

About a month later, after the patient was up and 
about the house daily, his wife was awakened early one 
morning by noting that the patient was breathing with 
difficulty. She arose to get him a glass of water and 
when she returned he was dead. 

Discussion .—In this case the presence of auricular 
fibrillation and the need for its control by digitalization 
were evident. There was much uncertainty of the pul¬ 
monary condition. Treatment was therefore undertaken 
for the relief of the heart failure. 

The sudden death was quite unexpected. Although 
the attending physician signed “cerebral hemorrhage” on 
the death certificate,.it is clear that at least two other possi¬ 
bilities must be considered. The discharge of an embolus 
from the heart to the lungs or brain may have taken place. 
A clotting of the blood, particularly in the auricular append- 


304 MODERN CONCEPTION OF HEART DISEASE 


ages, is not uncommon when the auricles are fibrillating. 
A rare possibility as a cause of this death is, perhaps, 
the onset of fibrillation in the ventricles. It has been 
noted experimentally, in animals, that sometimes when 
the auricles are fibrillating, the same mechanism may 
appear in the ventricles. Such an event probably occurs 
occasionally in human beings. In the absence of an 
autopsy the actual cause of death must remain unsettled. 

The diagnosis of hypertensive heart disease seems most 
probable from the two-year history of high blood pressure, 
the apparent hypertrophy of the heart, and the absence 
of the history or physical findings pointing to some other 
etiological type of heart disease. Finley 1 has reported 
heart changes as a result of a deformity of the spine of a 
considerable degree. In this case the condition of hyper¬ 
tension seems a sufficient cause, and I doubt the influence 
of the spinal deformity as a factor in this case. It is 
probable, however, that the pulmonary findings are ex¬ 
plainable in part, at least, by the deformity of the chest. 

THE HEART IN HYPERTHYROIDISM 

Case 15.—Housewife, aged forty-nine, born in Russia. 

Chief Complain t. —Nervousness. 

Past History .—Denies previous disease. Good health 
until four years ago, when home conditions became intoler¬ 
able. Husband became very abusive. After a few 
months the patient became nervous, and would jump at 
the slightest noise. Was advised at Psychopathic Hos¬ 
pital to take baths. Has done this for three years with 

1 Finley, F. G.: “Spinal Deformity as a Cause of Hypertrophy and 

Dilatation,” Canad. Med. Jour., xi, 10:79, Oct., 1921. 



ILLUSTRATIVE CASE REPORTS 


305 


apparent benefit, but always notes the return of the ner¬ 
vous feeling soon after reentering her home. 

Was a patient in the hospital two months ago. Com¬ 
plaint then was that the heart had been “jumping” for 
three months and there was dyspnoea and palpitation on 
exertion. She was very nervous and tired. The cata¬ 
menia had ceased about two months. 

The physical examination during this stay in the hos¬ 
pital was essentially normal save for a thrusting apex beat 
accompanied by a systolic thrill. The blood pressure was 
190/89, and the pulse rate eighty to one hundred. The 
electrocardiogram showed sinus arrhythmia and a rate of 
one hundred and fifteen to one hundred and twenty-five. 
On discharge the diagnosis was: menopause, hypertension. 

Present Illness .—Since leaving the hospital five weeks 
ago the nervousness has increased. Also the dyspnoea and 
palpitation on moderate exertion, such as walking up one 
flight of stairs, has increased. One month ago a dry cough 
and swelling of the ankles appeared. 

Patient noted a swelling in the neck (region of the 
thyroid) about six months ago. Perspiration is very free. 
There has been a loss of twenty-five pounds’ weight in the 
past year. The monthly periods are still absent, now four 
months. 

Physical Examination. —Thin, very restless woman, 
mentally clear. The eyes show no signs of Graves’s dis¬ 
ease. The thyroid gland is readily visible and palpable, 
and over it there may be heard a bruit. There is a visible 
pulsation of the carotid arteries. Well-marked fine tremor 
of hands. Skin warm and moist. 

Heart .—Heaving impulse in fifth space one centimetre 


20 


306 MODERN CONCEPTION OF HEART DISEASE 


outside left midclavicular line. By percussion left border 
is about 0.5 centimetre further to left; right border meas¬ 
ures 3.5 centimetres from the midsternum. No thrill. 
Action rapid and irregular. There is a systolic murmur 
loudest at the apex and transmitted over the precordia. 

The lungs are clear. There is slight soft edema of 
the ankles. Blood pressure measures 145/90. 

The electrocardiogram shows auricular fibrillation with 
a ventricular rate of one hundred and sixty-five to one 
hundred and eighty-five. 

After a few days’ administration of digitalis, a second 
electrocardiogram showed the same mechanism at a rate of 
one hundred and twenty-five to one hundred and thirty-five 
and a flattening of the T wave. 

The basal metabolism was 61.7 per cent., and after a 
few days a second test showed a rate of 61.2 per cent. 

Diagnosis. —Hyperthyroidism, auricular fibrillation. 

Discussion .—During the first stay in the hospital it 
was noted that at times the heart action was rapid and 
irregular and then a more normal rhythm returned. The 
first electrocardiogram was not taken during the rapid 
rhythm. It is possible that what the interne described were 
transient attacks of auricular fibrillation. The latter has 
apparently become fixed. 

In view of the later findings and the height of the basal 
metabolism on two occasions, the diagnosis of hyperthy¬ 
roidism would seem clear. Otherwise the case would be 
one of auricular fibrillation of unexplained origin. The 
lowering of the blood pressure after the establishment of 
the fibrillation is to be expected; also the record is less accu¬ 
rate than when normal rhythm obtains. 


ILLUSTRATIVE CASE REPORTS 307 

THE HEART IN DIPHTHERIA 

Case 16.—Roy, eleven years of age. Admitted to the 
South Department of the Roston City Hospital on October 
9, 1921. Diagnosis,—faucial diphtheria. October 10, pro¬ 
fuse watery muco-gelatinous discharge from right nos¬ 
tril, membrane lining right nasal cavity; left side clear, no 
discharge. Throat entirely filled with edema and mem¬ 
brane. Tonsils completely covered with a grayish-white 
raised membrane, which extends y 2 centimetre on to ante¬ 
rior pillars and on to soft palate on left for distance of about 
two centimetres. The posterior pharyngeal wall is com¬ 
pletely obscured. Breathing through the nose is entirely 
prevented. There is a marked edema of neck, more 
marked on left side; patient very toxic. 

The heart sounds are of fairly good quality. 

October 11.—Slight improvement in membrane, edema 
a little less. Heart sounds and pulse are somewhat weak¬ 
ened. Patient less toxic. Epistaxis for five minutes with 
a spontaneous cessation. 

October 12.—Membrane rolling up. Patient less toxic. 
Suggestion of presystolic roughening; regular rhythm. 

October 13.—Process is subsiding very definitely. 
Splitting of first heart sound but no suggestion of a pre¬ 
systolic roll. 

October 16.—Normal temperature. Membrane nearly 
all gone. Edema of neck now much less. Heart sounds 
good. 

October 20.—Throat no longer sore, edema of neck 
gone. Heart sounds of good quality, no evidence of 
cardiac enlargement. 

Patient vomited this a.m. 


308 MODERN CONCEPTION OF HEART DISEASE 


October 21.—Patient was very uncomfortable last night 
and had a weak, irregular pulse. This morning the heart 
sounds are regular and of good quality but vary frequently. 

General condition good. No evidence of palatal paraly¬ 
sis; knee jerks present. 

October 23.—Blood pressure better. No evidence of 
paralysis. The heart sounds are weaker with an occa¬ 
sional extrasystole. 

October 25.—Heart regular, no splitting of first sound 
or extrasystoles. 

October 31.—Heart 3.5 by 8.5 centimetres. Action is 
very irregular, at times without any regular sequence of 
rhythm, occasionally a few extrasystoles, and again a 
nearly normal rhythm. Four-sound gallop made out 
several times. 

November 1.—Heart slightly enlarged, absolute irreg¬ 
ularity of the beats. At times there is a splitting of the 
first sound and a typical gallop rhythm, and at other times 
four beats. 

November 3.—Heart is absolutely irregular, rate 140 
to 160. Diffuse apex impulse in fourth and fifth spaces 
just outside nipple line. Tenderness over the liver and in 
the epigastrium. Lips are slightly cyanotic; the ex¬ 
tremities moist. 

Examination shows a fairly strong but varying impulse 
in fourth and fifth spaces just inside the nipple line. Area 
of dulness not made out as enlarged. 

Great irregularity in strength and rhythm of heart 
sounds, absolute irregularity but with periods, estimated 
as part of a second, during which there is a series of rapid 
regular beats, and at times a semblance of gallop rhythm. 


ILLUSTRATIVE CASE REPORTS 


309 


Patient’s color is very pale, the lips are ashy and at 
times slightly cyanotic. Skin cool. Seven-thirty p.m.— 
Vomited again. At times the pulse pressure is only eight 
millimetres of mercury, but now is twenty-six millimetres. 

November 5. —Cheyne-Stokes respiration present last 
night and this morning. The gallop rhythm is still pres¬ 
ent but less marked and the heart sounds are stronger. 
Vomiting is occurring three to five times per day. 

November 7.—Condition about same, heart more regu¬ 
lar, now has a loud systolic murmur over precordia. There 
are some moist rales at base of the lung. Patient is not 
vomiting but has received nothing but small amounts 
of water. 

November 9.—Better. Doesn’t complain of precordial 
or epigastric distress. 

The heart sounds are somewhat irregular but of good 
quality. Fewer rales at the pulmonary bases; respiration 
normal. Pulses of very low tension. 

November 13.—Continues to improve. The heart 
action has gradually become regular and the sounds are of 
good quality. No further vomiting. Sleeps fairly well 
without morphia. 

November 14.—Regular rhythm with typical four 
sound gallop. No evidence of cardiac enlargement. 
Liver edge just below costal margin. 

November 18.—No murmurs over heart. Occasional 
extrasystoles. Knee jerks absent. There is considerable 
emaciation of the tissues. 

November 22.—Heart sounds normal. Pulse of fair 
tension. 

December 16.—LTp in chair for one hour. 


310 MODERN CONCEPTION OF HEART DISEASE 


December 19.—Abscess on thigh drained. This is ap¬ 
parently the site of former hypodermic injection. The 
culture showed no growth. 

December 26.—The knee jerks have returned slightly. 

January 13.—Up and about. Heart appears normal. 
Patient is still thin and somewhat weak. The heart rate 
accelerates with exercise but promptly returns to normal. 
Discharged from hospital. 

May 2.—Patient returned for examination. 

Heart .—Apex in fifth space just inside nipple line. 
Sounds clear, no murmurs, action regular. Rate—at rest, 
eighty; after hopping fifteen feet, ninety-six; one minute 
afterward, seventy-two; after hopping thirty feet, eighty; 
one minute afterward, sixty-eight. Tires easily. 

The electrocardiogram, on January 26, was normal in 
all respects. 

Diagnosis .—Faucial and nasal diphtheria, severe toxic 
disturbance of the heart, recovery. 

Discussion .—I am indebted to Dr. E. H. Place for the 
above case history, which I have abstracted somewhat fully, 
as it offers a striking picture of the functional disturbances 
which may be met in severe diphtheria. Electrocardio¬ 
graphic records were not procurable until the patient 
was fully convalescent, but the bedside notes are quite 
satisfactory. 

This patient was very toxic at the time of admission, 
and in view of the extensive amount of diphtheritic mem¬ 
brane that was present, it could confidently be expected 
that the heart would later show serious disturbance. Dur¬ 
ing the first three weeks the cardiac findings were those of 
a minor type, as changes in the first heart sound, variations 


ILLUSTRATIVE CASE REPORTS 311 

in rate, extrasystoles, etc. By October 31, an inconstant 
gallop rhythm was noted. On the third of November the 
description of the rhythm is that of auricular fibrillation. 
The low pulse pressure, at one time measuring but eight 
millimetres of mercury, is noteworthy. In early November 
the gallop rhythm was present much of the time for several 
days. This rhythm, as occurring in diphtheria, is nearly 
always due to heart-block. 

The result of the exercise test performed in May, nearly 
three months after the patient’s discharge from the hos¬ 
pital, is interesting; as is also the normal electrocardiogram 
taken on January 26. These points conform to the rule 
that if the patient survives he ultimately makes a complete 
clinical recovery. 2 

CONGENITAL HEART DISEASE 

Case 17.—A baby dying on the ninth day. 

History .—Weighed seven pounds and ten ounces at 
birth. Delivered by the operation of intermediate forceps; 
pituitrin was not used. Was not a blue baby. Nursed 
irregularly, well at some feedings and poorly at others; 
inclined to be drowsy and cried little. Definite cyanosis 
was never present, but there was a slight tendency to cya¬ 
nosis when the baby cried. On the fifth day there was 
quite marked jaundice, which had cleared in part at the 
time of death. The heart appeared normal on examination. 

At the 6 p.m. nursing period on the eighth day, the 
baby took the breast poorly. At 12 p.m., respiratory diffi¬ 
culty and cyanosis were noted. Death occurred at 5 a.m. 
of the ninth day. 

Family History. —Mother, aged thirty-five years, in 


2 Exception to this has been mentioned in chapter xiii. 



312 MODERN CONCEPTION OF HEART DISEASE 


good health, married seven years. No other children. 
There was one miscarriage, cause unknown, at two months, 
about five years ago. At the sixth week of this pregnancy, 
miscarriage was threatened by slight flowing for ten days. 
There was considerable morning sickness; the pregnancy 
then proceeded normally. Father, aged thirty-five, in 
good health. 

Autopsy. Heart .—The right side is large and full of 
blood, while the left cavities are almost empty. The right 
ventricular wall is distinctly thicker than the left. The 
upper third of the interventricular septum is absent, and 
the opening thus formed is continuous with that of the 
foramen ovale between the auricles. The annulus from 
the posterior wall of the left auricle is present but is not 
adherent to the margin of the foramen ovale. The mitral 
and tricuspid valve flaps are almost in contact as they 
descend into the ventricles. The ductus arteriosus is freely 
patent. There is a constriction, amounting almost to 
obliteration, in the aorta at a point one half inch before it 
is joined by the ductus arteriosus. 

The liver shows beginning central necrosis. 

There is a blind pouch in the small intestine leading to 
the umbilicus. This is probably a Meckel’s diverticulum. 

Diagnosis .—Congenital heart disease, patent inter¬ 
ventricular septum, patent ductus arteriosus, coarctation 
of the aorta, beginning central necrosis of the liver. 

Discussion .—The unexpected death of this infant was 
not explained until the autopsy had been performed. 
Otherwise it might have been thought to have been a 
delayed result from the operative delivery. Emphasis is 
laid upon the extensive abnormality in the heart and 


ILLUSTRATIVE CASE REPORTS 


313 


adjacent vessels without the presence of evidence sufficient 
to make possible the diagnosis before death. 

The greater thickness of the right ventricular wall is 
the rule at birth. Also, since the ductus arteriosus was still 
freely patent, it was not surprising that there was no evi¬ 
dence of the adhesion of the annulus to the margin of the 
foramen ovale. The constriction of the aorta was probably 
unimportant, as the blood would doubtless have been con¬ 
veyed by the development of collateral vessels. The 
change in the liver cells is most likely due to the imperfect 
arterial blood which must have resulted from the abnor¬ 
malities in the heart and vessels. 

"Whether the threatened miscarriage at the sixth week 
had any influence in the failure of development of the 
interventricular septum is, of course, an open question. 
It is noteworthy that the aortic part of the septum should 
have been forming at about this time and the septum should 
have been complete before the end of the third month. 

Case 18 .—Twenty-year-old girl, single. 

Family History .—Father and mother dead, cause 
unknown. One sister died at the age of twenty-four of 
pulmonary tuberculosis. Another sister is living and well. 

Past History .—Scarlet fever when child; otherwise 
recalls no illness. Could run and play with perfect 
freedom. 

Present Illness .—When undergoing a physical exam¬ 
ination preliminary to the acceptance of employment with 
the United Fruit Company, an abnormality in the position 
of the heart was discovered. There are no symptoms of 
disease or departure from normal health. 

Physical Examination .—Well developed and nourished. 


314 MODERN CONCEPTION OF HEART DISEASE 


Heart .—Impulse in fifth space just inside right mid- 
clavicular line. By percussion heart is located to right 
rather than left of sternum; right border of heart is 7.5 
centimetres to right of midsternum and left is 3.5 to left. 
Liver dulness apparently present on left side from sixth rib 
to costal margin, where its lower edge is just palpable. 
Examination otherwise normal. 

Rontgen examination shows transposition of thoracic 
viscera. 

The electrocardiogram is normal save for an inversion 
of all waves in lead I. 

Diagnosis .—Congenital heart disease, dextrocardia. 

Discussion .—The abnormal position of the heart is but 
part of a general transposition of the viscera. The inver¬ 
sion of all the waves in lead I of the electrocardiogram is 
diagnostic of congenital dextrocardia and is a differential 
point from dextrocardia acquired after birth. The condi¬ 
tion of congenital dextrocardia is compatible with health. 

EFFORT SYNDROME: IRRITABLE HEART 

Case 19.—A returned soldier, aged thirty years. 

Past History .—Excellent health. Recalls no illness 
until time of army service. Was gassed in battle in Sep¬ 
tember, 1918. Received skin burns, of first degree, which 
healed in about six weeks. Also vomited a few times 
after being gassed. There was aphonia for six weeks. 
Kept in bed for about five weeks because of palpitation of 
the heart. Cough, sputum, and fever for a few days. 
Remained in the hospital nine weeks in all. 

Patient returned to duty for two months. In February, 
1919, on awakening one morning, he noted a sharp pain 
in the right side. He was sent to a base hospital for four 


ILLUSTRATIVE CASE REPORTS 315 

v eeks, three ot which were spent in bed. Fever, with tem¬ 
perature of 103° to 104°, was present for three to four 
days. Is early had pneumonia.” There was a tendency to 
palpitation at the time of discharge from the base hospital. 

Present Illness. —Since his return from France and 
return to civil life two months ago, the patient has been 
troubled somewhat by palpitation, particularly on retiring 
at night. He has tried a little hill-climbing in the past 
two weeks and noted moderate amount of palpitation. 
Four days ago there was a slight return of distress in the 
right side (axilla) ; no cough or other symptoms. Other¬ 
wise feels in good health. 

Physical Examination. —Slight pyorrhea. Lungs nor¬ 
mal to percussion and auscultation. 

Heart. —Measures 3 by 9.5 centimetres, about one 
centimetre outside nipple line. Action regular, rate 
eighty-two. First sound at apex is snapping in quality; 
pulmonic second sound not accentuated; no murmurs. No 
tremor of fingers. 

Diagnosis. —Effort syndrome. 

Discussion. —This case is similar to many others found 
in the army. The signs and symptoms, essentially those of 
a lack of physical fitness, and the history of being gassed, 
and of “nearly having pneumonia” two months before I 
examined him, offer a sufficient reason for the condition 
termed effort syndrome. The history contains some de¬ 
tails by which one may judge as to the probable severity 
of the gassing and of the respiratory affection. In the 
absence of other findings of abnormality, I do not put much 
weight on the left border of cardiac dulness being one 
centimetre outside the nipple line. 


316 MODERN CONCEPTION OF HEART DISEASE 


The pain in the right side may be due to pleural adhe¬ 
sions resulting from the chest infection. The possibility 
of this and the nature of effort syndrome was explained 
to the patient. He was advised as to regular exercise 
to regain his physical fitness. He rapidly returned to 
good health. 

Case 20. —Housewife, aged thirty-two years. Referred 
with the diagnosis: “ Myocarditis.’’ 

Past History .—Influenza three years ago. Attacks 
similar to the present when in high school, and three years 
ago when last baby was born. 

Present Illness .—Palpitation and faintness during the 
past two years. The duration is about ten minutes, and 
the cessation is gradual. Sometimes has the sensation as 
if the heart turned over. One flight of stairs causes no 
shortness of breath, if taken at an ordinary pace. Occa¬ 
sionally has pains, mostly occurring at the times of the 
menses. The attacks or symptoms are usually associated 
with nervous excitement. Feels she has had much trouble 
and reason to be nervous. 

Physical Examination .—Fairly well developed, some¬ 
what thin (weight one hundred and seven pounds). 

Heart .—Impulse palpable in fifth space in left mid- 
clavicular line; no enlargement to percussion. At the 
apex there is a faint systolic murmur with the first sound; 
no diastolic murmur appreciated. Pulmonic second sound 
is louder than aortic second but is not accentuated. 
Considerable respiratory arrhythmia; heart rate about 
eighty-two. 

Social History. —Children: Frederick, eleven years, six 
months; Eleanor, eight years, eight months; Pearl, two 


ILLUSTRATIVE CASE REPORTS 317 

years, six months. Both little girls appear lovable and 
fairly healthy; normal births. Birth of the boy was normal, 
but mother was under quite a nervous strain during preg¬ 
nancy. Husband developed peculiarities shortly after she 
was married; was abusive to her during the first pregnancy. 
He continued this abuse through ensuing years and showed 
terrific temper, especially toward the boy, whom he fre¬ 
quently struck. Husband was committed to Psycho¬ 
pathic Hospital in 1916, sent to Westboro, and discharged 
in 1917. He came home and resumed his abuse toward 
his wife and son. Mother tried to have him arrested two 
or three times but changed her mind. The boy became 
cowardly, depressed, and prematurely old, while the mother 
became very nervous and easily upset. 

In July, 1920, a visitor from the Boston Children’s 
Aid Society went to the home and found the mother ill 
on a couch from the effects of the husband’s brutality. 
She said he had knocked her down, kicked and stepped on 
her with heavy shoes, causing severe bruises; eye-glasses 
were broken and she was unable to get about. The hus¬ 
band was arrested and sent to the Cambridge Jail, where 
he was bailed out by his employer. He was later found 
guilty and placed on probation. In December, 1920, the 
court case was placed on file. 

The patient had been examined by Dr. D— (an out¬ 
side physician), who stated that she is a delicate, nervous 
woman, hypochondriacal and ana 2 mic. He had treated her 
principally for pelvic irritation, due to the fact that she 
had not received proper care after the birth of her child. 

Our contact with the patient has been one of fairly 
good cooperation, but we have felt that she never had a 


818 MODERN CONCEPTION OF HEART DISEASE 


proper environment in which to get well. Mr. S— was 
arrested again in September, 1921, was found guilty of 
non-support of his wife and children, and of being armed 
with a dangerous weapon. He was given eight months’ 
sentence and was committed to the House of Correction. 
On November 1, 1921, the patient was operated on for 
complete hysterectomy and has gotten along well, but is 
worried about the approaching return of her husband 
from jail. 

(The above lengthy social history may seem irrelevant 
to the subject of cardiology, hut is quoted with the object 
of illustrating the futility of treating such cases from a 
purely medical standpoint.) 

Diagnosis .—Irritable heart. 

Discussion .—When this patient was first seen before 
the social history was obtained, my note on the record reads: 
“No evidence of true heart disease. Proper term is prob¬ 
ably ‘irritable heart’ ( i.e ., a normal heart in a nervous 
person). Environmental troubles could cause all these 
symptoms.” It was hardly expected, however, that such 
a chapter of troubles would be disclosed. Can it be won¬ 
dered that the patient was upset nervously? It would 
seem that the diagnosis obtains much support. 

It has been my experience, when making the diagnosis 
of so-called irritable heart, to so frequently find in the 
social history data which might reasonably have given rise 
to the symptoms, that in all such cases an exploration of this 
part of the history is suggested. The above case well 
illustrates the value of so doing. Such patients are often 
sent to the heart specialist as probable cases of heart disease. 

The diagnosis, “Myocarditis,” is unjustifiable; there is 


ILLUSTRATIVE CASE REPORTS 319 

nothing in either the history or the examination to indicate 
real heart disease. The term “myocarditis” was probably 
employed, as is not infrequently true, because the physician 
thought there was something wrong with the heart, but 
could not find sufficient data on which to base the diagnosis 
of a valvular lesion. A diagnosis of this sort leads to 
nothing helpful and may even cause the overlooking of 
facts such as those brought out in the social history. It 
would be preferable to label such a case, “Probable heart 
disease, type undetermined,” as this would stimulate fur¬ 
ther effort toward diagnosis. 

MISCELLANEOUS CONDITIONS 

Case 21. —Banker, aged fifty-four years. 

Complaint .—Shortness of breath if walks rapidly, and 
some pain in left arm. 

Family History .—Wife and one daughter in good 
health. No children dead; wife has had no miscarriages. 

Past History .—Jaundice twenty-five years ago; com¬ 
plete recovery in a few weeks. At the age of twelve patient 
had a short attack of asthma. Denies other diseases when 
named in order. Four years ago, there was an attack of 
pain in the right flank; diagnosis that of renal stone. 
Advised to discontinue coffee and meat and has felt better. 
Now uses a little meat. Formerly was a hearty eater, 
including much meat. 

The patient has been under considerable business 
strain. Five months ago he was all used up from over¬ 
work; felt better after several days’ rest. Inclined to 
active exercise. He has never smoked, and has taken 
almost no alcohol. There has been a gain of ten pounds’ 
weight in the past year. 


320 MODERN CONCEPTION OF HEART DISEASE 


Present Illness .—While climbing a mountain last sum¬ 
mer patient noted a pain along the inner aspect of his left 
arm. Soon better and was able to continue the climb. 
Seven weeks ago he played four sets of doubles at tennis 
without apparent trouble. 

During the past six weeks, however, when walking 
rapidly, there has been a distress under the head of the 
sternum. The sensation is described as “ like that one gets 
after running too much.” It is often associated with a 
similar distress over the left pectoral muscles and down the 
inner aspect of the left arm to the elbow. During the attack, 
wdiich persists two to five minutes, he stops ostensibly 
to look in a store window. States that these attacks are 
so frequent that he has ceased taking the train to town, 
and goes by trolley so as to avoid meeting his numerous 
business friends and to be able to walk the few blocks to 
his office alone and at his own pace. Has noted, however, 
that sometimes if he is walking with some one and engaged 
in conversation, he may escape an attack. 

Patient states that he has several times recently been 
told by other physicians that he was all right, and comes 
expecting he would be given a clean bill of health. (Much 
of the data listed above was obtained only by spending 
considerable time in taking the history, although the latter 
was not given unwillingly.) 

Physical Examination .—Very well-developed man, not 
overweight. Pupils equal and react to light and distance. 
Teeth in good condition. No general glandular en¬ 
largement. 

Heart .—Supracardiac dulness two by one and one half 
centimetres. No visible or palpable pulsation in the supra- 


ILLUSTRATIVE CASE REPORTS 


321 

sternal notch. Impulse barely palpable one finger’s 
breadth outside the nipple in the fifth and sixth spaces. 
Action regular, no murmurs, aortic second sound slightly 
accentuated. Heart rate seventy-two. Blood pressure; 
systolic one hundred and sixty, diastolic one hundred and 
ten. No suggestion of alternation noted (in taking 
blood pressure). 

Urine clear, slightly acid, 1024, albumen and sugar 
absent. 

Rontgen examination. Heart appears normal in size 
and contour, though there is a doubtful suggestion of 
enlargement of the left ventricle. The aorta appears 
elongated with a marked prominence of the knob to the 
left. Fluoroscopic examination not made. 

Diagnosis .—Probably hypertensive heart disease. 
Definite angina pectoris. Some cardiac enlargement 
probable. 

Discussion .—The above is clearly a case of angina 
pectoris. This diagnosis is based almost entirely on the 
history, which is consequently given somewhat in detail. 
The story of the patient’s endeavor to walk alone, so as to 
be able to take his own pace, is quite impressive in the 
case of a man who has until recently played tennis 
with pleasure. 

An etiological diagnosis of hypertensive heart disease 
is suggested by the blood-pressure record and the probable 
slight enlargement of the heart. Of course, before the 
diagnosis of hypertension can be definitely accepted, it must 
be shown that the blood-pressure levels are constantly ele¬ 
vated. Also a Wassermann test should be made and per¬ 
haps antisyphilitic treatment instituted. The presence of 
21 


322 MODERN CONCEPTION OF HEART DISEASE 


cardiovascular syphilis must be considered because of 
the angina pectoris, but not, however, because of the 
hypertension. 

This patient was seen but once prior to his going abroad. 
The presence and nature of angina pectoris was explained 
to him and, together with other advice, the need of addi¬ 
tional examination was pointed out and apparently ac¬ 
cepted. This man’s history is cited partly as an illustration 
of the uncertainty as to the etiological type of heart present 
in some of our cases and the need of carefully watching 
such cases in order that disease may be recognized in its 
earliest phases. 

Case 22. —Widow, twenty-one years of age. 

Complaint .—Pain over heart. Is said to have angina 
pectoris. 

Past History .—The patient recalls practically no dis¬ 
eases. She was subject to weakness and fainting attacks 
during her childhood. At the age of fifteen the patient 
was married to a much older man; the marriage was ar¬ 
ranged by her mother for financial reasons. There devel¬ 
oped soon after a condition described as “nerves.” Often 
the patient fainted from worry. She lived but eight months 
with her husband, who was later killed in an accident, and 
then for two years the patient was free from “weak spells.” 
She has been a dancer and living a life of social excess. 
Denies venereal disease. 

Present Illness .—About eight months ago, at night 
after a dance, a twinge was felt round the heart and the 
patient fainted. The next morning there were eighteen 
such attacks of a duration of two to three minutes. Two 
weeks later twelve similar attacks occurred while the pa- 


ILLUSTRATIVE CASE REPORTS 323 

tient was sitting in a chair. She did not definitely faint 
each time. With the first attacks the patient would stiffen. 
“As long as the pain keeps down I can get the better of 
it, but when it comes up (put hand over second left costal 
cartilage) I can’t get my breath.” The pain is described 
as gripping or squeezing; it does not radiate to arms, 
shoulders, or back. Ascending stairs causes palpitation 
for about ten minutes. A sensation of fatigue is present 
in the morning; the patient feels fine at times and down 
in the dumps shortly after. 

For the past three weeks the patient has been kept in 
bed, but is not improving. Attacks of pain recur at irregu¬ 
lar intervals, never following exertion. 

Physical Examination .—Young woman, well devel¬ 
oped. Pupils equal and react to light. Teeth in excellent 
condition. Tonsils appear normal. No general glandu¬ 
lar enlargement. 

Heart .—Impulse in fifth space inside left midclavicular 
line. No increased supracardiac dulness, percussion out¬ 
line of the heart is within normal limits. Sounds clear, no 
murmurs, regular rhythm. 

Reflexes normal. No skin lesions, thickening of tibiae, 
or other signs to suggest syphilis. 

Further History .—The friend at whose home the pa¬ 
tient is visiting states that at the time of the attacks, the 
patient runs screaming round the house and will hurt 
herself unless prevented. At times it takes several per¬ 
sons to hold her in bed. 

Family physician reports that the patient is in love with 
a young man of her own age, but is probably to marry an 
older man who has more money. 


324 MODERN CONCEPTION OF HEART DISEASE 


Wassermann test negative. 

Rontgen examination shows a heart and aorta of normal 
contour and size. 

Diagnosis .—Not true angina pectoris, or true heart 
disease. 

Discussion .—At the age of twenty-one angina pectoris 
is of very rare occurrence. In the above case history, it 
should be noted that the attacks are not associated with 
exertion, but with emotional stimuli. The picture is that 
of a functional nervous condition, for which ample causa¬ 
tion is found in the patient’s history. The negative 
Wassermann reaction and normal Rontgen findings are of 
confirmatory value in excluding true angina. The scream¬ 
ing and activity of the patient during the attacks should 
immediately suggest that some other condition than true 
angina pectoris is present. This detail of the history 
would probably not have been obtained if a description 
of the attacks had not been sought from others than 
the patient. 

The reason why this was not a real disease of the heart, 
but rather a nervous condition resulting from her numerous 
troubles, was explained in some detail to the patient, who 
appeared ready to listen carefully. The desirability of 
leading a more normal life was pointed out. Her physi¬ 
cian reported that the attacks ceased and there was a rapid 
return of the patient’s usual strength. 

The above case forms a good contrast to Case 21. 

Case 23. —Housewife, forty-six years of age. Entered 
hospital for treatment of erysipelas of the face, chest, 
and arms. 

Past History .—Measles when child; otherwise has en¬ 
joyed good health. 


ILLUSTRATIVE CASE REPORTS 


325 


Present Illness .—Erysipelas started on the face and 
later extended to the chest and arms. Fever, varying from 
101° to 104°, continued about sixteen days. Patient be¬ 
came much debilitated. 

Three weeks later, pain in the joints and nodules in the 
superficial tissues of the limbs appeared; a diagnosis of 
erythema nodosum was made. 

Toward the end of the eighth week (when the writer 
first saw this patient), the heart rate was showing marked 
variations, from normal to one hundred and fifty per 
minute. The periods of tachycardia occur several times 
per day and persist for several hours. (Three weeks ago 
a similar condition of regular tachycardia was present at 
intervals for about ten days.) 

Physical Examination .—Fairly well developed and 
nourished. Moderate cyanosis of face, lips, ears, and 
fingertips; patient looks uneasy and complains of a pain 
in the right epigastrium. Cervical veins engorged and 
pulsating rapidly. 

Heart .—Impulse barely palpable in fifth space at left 
midclavicular line. Borders of deep cardiac dulness within 
normal limits. Action regular, rate one hundred and 
fifty-six per minute; sounds tick-tack in quality, no mur¬ 
murs appreciated. 

Pulses barely palpable, regular, rate one hundred and 
fifty-six. 

The liver extends from the sixth rib to three fingers’ 
breadth below the costal margin in the mammillary line. 
The lower edge is distinctly tender on palpation. There 
is no edema of the extremities. 


326 MODERN CONCEPTION OF HEART DISEASE 


Digital pressure on the right vagus nerve in the neck, 
combined with the holding of a deep breath by the patient, 
slowed the heart rate markedly for a few seconds. On the 
sixth attempt, the heart rate suddenly dropped to eighty- 
two and remained at about that level. This was promptly 
followed by a radial pulse of normal rate and volume, 
disappearance of the engorgement of the cervical veins 
and the cyanosis of the face, and very evident relief to 
the patient. 

The electrocardiogram, taken just previous to the use 
of pressure on the vagus, showed paroxysmal tachycardia 
of auricular origin. The tracing is reproduced in Fig. 20. 

Diag n osis .—Paroxysmal tachycardia. 

Discussion .—The successful abolition of the paroxysm 
required repetition of the methods used. There was evi¬ 
dently a considerable degree of circulatory failure, all of 
which, including the enlargement of the liver, disappeared 
after the return of normal rhythm. 

The etiologic diagnosis is uncertain. The occurrence 
of the infections noted in the history offers a sufficient cause 
for this functional disturbance of the heart. Whether the 
latter was affected by toxins or was directly infected could 
best be determined at a future date. The paroxysms 
ceased and therewas no further evidence of cardiac disturb¬ 
ance. It would be a good plan to examine such a patient 
after the lapse of a few months. 

Case 24.—Boy, aged four and one half years. 

Complaint .—Very slow heart rate, and the possibility 
of convulsions. 

Present Illness .—There is a history of convulsions 
which occur in the morning and last for a few minutes, 


ILLUSTRATIVE CASE REPORTS 


327 


after which the patient appears normal. No other symp¬ 
toms. He appears to be well and strong. Brought to 
a physician for treatment of the convulsions. On examina¬ 
tion the heart rate was found to be about forty per minute, 
but on exercise the rate promptly doubled. Exercise is 
well tolerated. The physician suspected A-V heart- 
block and referred the patient for electrocardiographic 
examination. 

Family History .—Contains no pertinent data. 

Past History .—Patient had a normal birth and was 
breast-fed. There have been no previous illnesses. 

Physical Examination .—Well developed and nour¬ 
ished. Reflexes normal. Teeth, tonsils, and glands 
normal. 

Heart .—The impulse is in the fifth space just inside 
the nipple line; the borders of dulness are within normal 
limits. Sounds clear, no murmurs appreciated. When 
the patient is sitting quiet the heart rate is about forty-four 
per minute, but the rate promptly becomes about eighty if 
he stands up or exercises. The action is essentially regular 
save for the change of rate. There are no visible waves in 
the cervical veins during the long diastoles of the heart. 
The pulses are of good volume and tension; there is no 
pulse deficit. 

The electrocardiogram shows sino-auricular block. At 
the slow rate the rhythm originates in the auriculo- 
ventricular node, and in the sinus node at the faster rate, 
i.e. } there is a shifting of the pacemaker. The P-R interval 
measures 0.14 second. 

Diagnosis. —Sino-auricular block. 

Discussion .—This is an example of a functional condi- 


328 MODERN CONCEPTION OF HEART DISEASE 


tion of the heart of unknown origin, and, in the absence of 
other evidence of abnormality in the heart, should not be 
interpreted as proof of disease. It must in no sense be 
confused with true heart-block, i.e between the auricles 
and ventricles, an error that was made by his physician after 
receiving the report of the electrocardiogram. 

The entire lack of the symptoms and signs of heart 
failure in this patient should suggest an essentially normal 
heart. The approximate doubling and later halving of the 
heart rate is a well-known sign of sino-auricular block. The 
normal appearance of the venous pulse is helpful to those 
accustomed to using this finding. 

There is no doubt that, in a case such as the above, the 
electrocardiogram is of distinct value in establishing the 
diagnosis. It may be noted that the nature of the convul¬ 
sions has not been discussed. Observation in a hospital for 
a period of ten days failed to show anything abnormal. 

Case 25. —Married woman, aged twenty-four years, 
born in the West Indies. 

Complaint .—Palpitation and fainting. 

Present Illness .—Patient is referred from the Mater¬ 
nity Clinic of the Boston Homeopathic Hospital. 

There has been a tendency to a rapid heart rate (patient 
indicates by motion of the hand a rate estimated to be about 
one hundred) and fainting. The pregnancy is now in the 
fourth month; there has been much morning sickness with 
vomiting, but recently this has ceased. 

Past History. —Measles, whooping cough, and an occa¬ 
sional mild sore throat are the only diseases recalled. 
Otherwise the patient has enjoyed good health; could run 
and play well. 

Physical Examination .—Well developed but thin. 


ILLUSTRATIVE CASE REPORTS 


329 


Heart .—The impulse is palpable in the fifth space 
inside the left midclavicular line; percussion borders within 
normal limits. There is a soft systolic murmur with the 
first sound at the apex; the sounds are otherwise normal. 
Some variation in rate with respiration is present. 

Electrocardiogram. During the taking of this the pa¬ 
tient fainted. She was placed in a horizontal position on 
a couch, and recovered in a few minutes. The record 
showed a normal sinus rhythm of a rate of about eighty- 
eight, before and after the attack; during the few minutes’ 
loss of consciousness A-V rhythm, rate sixty-nine, was 
present. 

Diagnosis. —Sino-auricular block interrupting normal 
rhythm. 

Discussion .—The patient was probably suffering from 
an irritable heart induced by the recent period of severe 
nausea and vomiting of pregnancy. The shifting of the 
pacemaker from the sinus to the A-V node was most likely 
due to the action of the vagus nerve. While the patient 
was unconscious the heart sounds were regular and of good 
quality; the slowing of the rate led to the conclusion that 
atrio-ventricular rhythm was present. 

Neither in the history nor in the electrocardiogram of 
this patient is there evidence of actual disease of the heart. 
It was predicted that the patient would be in good health 
as soon as the effects of her recent illness had disappeared. 

Case 20. —Hospital interne, twenty-eight years old. 

Complaint .—Irregular heart action occurring during 
an acute nasal sinusitis. 

Past History .—He has had measles when an infant, 
typhoid fever at the age of eleven, and tonsillitis of five 
days’ duration about eight months ago. Otherwise has 


330 MODERN CONCEPTION OF HEART DISEASE 


enjoyed excellent health; has never noted any signs or 
symptoms of cardiac disturbance. 

Present Illness .—Four days ago there was a sudden 
chill followed by fever and an aching all over the body. 
Other symptoms are,—loss of appetite, moderate nausea, 
and a single attack of vomiting twenty-four hours ago. 
There has been a temperature ranging from 101° to 102° 
for four days. 

Yesterday tenderness developed over the right an¬ 
trum, and there is a feeling of fulness in the right cheek 
and forehead. Coryza was present two days before the 
chill, but has become much less since then. Marked irregu¬ 
larity of the heart has been present during the past 
twenty-four hours. 

Physical Examination .—Patient looks prostrated. 
There is a slight nasal discharge of a purulent type, mostly 
from the right nostril. 

Heart .—Impulse in the fifth space just inside the 
nipple line. The right border of deep cardiac dulness is 
two centimetres and the left border nine centimetres from 
the midsternum. There are no murmurs. The rhythm 
is a regular irregularity; coupling is often heard, and at 
times there are three or more regular beats interrupted by 
premature sounds. During the coupling, alternate large 
and small waves are readily distinguished by palpation of 
the pulse. Inspection of the venous pulse in the neck 
shows the auricular wave preceding the waves that are 
simultaneous with the beat following the longer pauses. 

The arteriogram shows premature beats alternating 
with normal beats. The tracing is reproduced in Figure 5. 

The electrocardiogram shows ventricular premature 
beats interrupting a sinus rhythm. 


* ILLUSTRATIVE CASE REPORTS 


331 


The antrum was drained and in two days the irregu¬ 
larity of the heart disappeared. Convalescence was 
uneventful. 

Diagnosis .—Acute sinusitis, ventricular premature 
beats. 

Discussion .—The picture is that of an acute infection 
of considerable severity. The appearance of extrasystoles 
is not uncommon in such cases. The condition is to be 
sharply distinguished from true pulsus alternans. A care¬ 
ful noting of the time of the beats, particularly on ausculta¬ 
tion, made it clear that some of the beats were premature; 
such would be the usual explanation of the coupling. Sino- 
auricular block, or true heart-block, with a dropping of 
every third beat, would be a possibility, but could be ex¬ 
cluded by the occasional runs of normal beats, which gave 
a gauge as to the usual interval that should separate the 
beats if all were of normal origin. Also the waves in the 
radial pulse showed a marked and regular alternation in 
volume, which is not a feature of dropped beats. By 
means of the data discussed in Chapter XVII it was easy 
to exclude sino-auricular block, or heart-block, and to con¬ 
fidently diagnose the extrasystoles. The graphic records 
were conclusive. 

This heart was doubtless affected by the acute general 
toxemia, but since the recovery was prompt and complete, 
an actual infection of the heart can be confidently dismissed. 

Case 27. —Lawyer, aged forty-five. 

Complaint .—Cyanosis and irregular action of the heart. 

Past History .—Has always enjoyed good health. 
Could run as well as other boys, but was not so strong. 
Was told, when about nineteen years old, that his heart was 
irregular and has received many opinions from different 


332 MODERN CONCEPTION OF HEART DISEASE 


physicians; some said the condition was harmless, and 
others, serious. The doctors are always examining his 
heart; the condition is called functional, as a rule. Patient 
noted that his heart was regular if he had fever. 

Present Illness .—During the past three years his 
friends have frequently commented upon the duskiness of 
his face and hands, though he himself was less conscious of 
any change in color. Has noted that after playing golf 
or being out in the air, the blueness of the skin is less prom¬ 
inent. Feels in excellent health, enjoys three sets of 
tennis, is now planning a fishing trip into the Maine woods. 
Referred for electrocardiogram. 

Physical Examination .—Well developed and nour¬ 
ished. Face and hands have dusky slate-colored tinge. 
This does not show accentuation at the lips and ears, or 
fingertips. The “cyanosis” is absent above the wrists and 
below the level of the collar; it is especially marked at the 
base of the nails, at the lunulse. The dusky hue is absent 
inside the mouth. On pressure the skin blanches, but a 
very definite bluish color remains. 

Heart .—Apex impulse in fifth space inside nipple line, 
no evidence of enlargement disclosed by percussion. Split 
first sound at apex. Regular rhythm frequently inter¬ 
rupted by premature beats, rate seventy-two. One hun¬ 
dred hops well tolerated; rate accelerated to one hundred 
and twenty and became perfectly regular. As the heart 
slowed, the irregularity returned at the rate of ninety. 
No edema. 

Diagnosis .—Premature beats, argyria. 

Further History .—No history of the use of silver 
nitrate. Some digestive trouble about ten years ago for 
which he took a liquid medicine, of red color, for a few 


ILLUSTRATIVE CASE REPORTS 


333 


months. Twelve years ago argyrol was prescribed for the 
treatment of a catarrhal condition of the nose. Patient 
liked the effect so well that, on his own initiative, he contin¬ 
ued the use of this at least twice a day for eight years. 
Is satisfied that he swallowed considerable of the drug. 
The change in the color of the skin appeared gradually, 
four years ago. 

The electrocardiogram showed premature beats of 
ventricular origin. 

Discussion .—The duskiness of this man’s face and 
hands was of the degree that is rarely present save in 
patients almost in extremis, and yet he admitted no impair¬ 
ment in health. In addition to this reason to question the 
genuineness of the cyanosis, a more careful examination 
showed, as described above, that it was abnormal in its 
distribution and its non-disappearance on pressure. It is 
noteworthy that the discoloration was limited to those 
parts of the body surface that are readily accessible to light; 
this patient stated that he rarely rolled up his sleeves or 
wore a bathing suit. In a sense the patient has become 
somewhat like a photographic plate. The most reasonable 
explanation of the lessening of the blueness of the skin 
after exercise in the open air is that the natural redness 
of the skin so induced tended to mask somewhat the under¬ 
lying pigmentation. 

Cases of argyria from the use of argyrol appear to be 
rare, but it is the probable offender in this case. Since the 
patient admitted the habit of swallowing the drug freely, 
it is the less surprising that argyria ensued. 

The cardiac irregularity presented all the clinical fea¬ 
tures of extrasystoles. This history of an irregularity for 
years, with the continuance of normal health and vigor, 


334 


MODERN CONCEPTION OF HEART DISEASE 


should suggest the arrhythmia to be of the simpler type. 
The rhythm became regular after acceleration of the rate 
by exercise; the patient had made a similar observation 
when fever was present, i.e., when the heart rate was 
increased. 

Case 28 .—Physician’s daughter, aged seven years. 

Chief Complaint .—Sent home by school physician with 
the report of heart disease. 

Family History .—Parents and two sisters living and 
well. 

Past History .—Whooping cough and chicken-pox one 
year ago. No rheumatic fever, growing pains, chorea, 
tonsillitis, or scarlet fever. Has always been strong; plays 
with girls of an older age; can run well. During the past 
two years has been kept out of school some because of 
being underweight. By means of a generous diet, more 
fresh air, and rest, she has gained weight in the past year. 

Physical Examination .—Fairly well developed and 
nourished. Mucous membrane of good color. Tonsils 
moderately prominent, no evidence of disease. Teeth in 
excellent condition. A few small, non-tender cervical 
glands. Thoracic wall very curving (moderate pigeon- 
breast). 

Heart .—Impulse in fifth space just outside of nipple 
line. Border of cardiac dulness appears within normal 
limits. Loud systolic murmur in second and third left 
interspaces near the sternum transmitted to right and 
into neck. This murmur is much diminished on full 
inspiration. Respiratory arrhythmia present. 

Hemoglobin, ninety per cent. 

Diagnosis .—No heart disease. 

Discussion .—The only suggestion of an affection of 


ILLUSTRATIVE CASE REPORTS 


335 


the heart is the murmur of maximum intensity at the 
pulmonic area. In the absence of other abnormal findings 
it is a safe dictum to disregard such murmurs. The causa¬ 
tion of this type of murmur is uncertain, but, in my opinion, 
if anemia is absent, the most probable explanation is the 
relation of the conus arteriosus and great vessels to the 
underlying thoracic wall. (See Chapter XIV.) It was 
noted that this little girl s thorax was somewhat abnormal 
in shape. 

Case 29.—Housewife, aged forty-two. 

Family History. —Unimportant. 

Past History .—Never well and strong. Best weight 
one hundred and six pounds, now is ninety-five. Recalls 
none of the diseases of childhood. 

Husband left her eight years ago. There are no chil¬ 
dren. Patient inclined to worry. Thought she had ac¬ 
quired syphilis from her husband, but there have been 
no symptoms in support of that diagnosis, and several 
Wassermann tests have been negative. 

Present Illness .—Some backache when she has been 
on her feet long. Also notes a drawing sensation as though 
a weight on the anterior abdomen. Comes to Heart Clinic 
as a case of probable valvular heart disease. A soft sys¬ 
tolic murmur has been found at the apex, and the patient 
is said to have shortness of breath and pain on exertion. 

Tires easily. 

* 

After careful questioning it is clear that the patient 
is not short of breath on exertion that is reasonable, in my 
opinion, for one of her sex, age, and physique. Also the 
pain is found to be that noted above, or rather, a drawing 
sensation in the epigastrium. This symptom is equally 


336 MODERN CONCEPTION OF HEART DISEASE 


liable to be present when the patient has simply been 
standing too long. 

Physical Examination .—Poorly nourished woman with 
stature conspicuously that associated with visceroptosis. 
The chest is flat, the costal angle narrow, the lower abdom¬ 
inal w T all sagging, and there is a prominent anterior curve 
to the lumbar spine. 

Heart .—The impulse is palpable in the fifth space at 
the midclavicular line; the percussion borders of the heart 
are within normal limits. Action regular, no definite mur¬ 
murs appreciated. The first sound at the apex is some¬ 
what crescendo in type. 

The pulses are of fair volume and tension. Blood 
pressure 130/85. Reflexes lively. 

Diagnosis .—Not true heart disease. Visceroptosis. 

Discussion .—The soft systolic murmur at the apex is 
probably what I have described as a crescendo type of first 
sound. It is known that in some normal hearts the first 
sound appears to begin with a soft murmur, or has a 
crescendo quality which closely simulates the type of first 
heart sound often present in cases of mitral stenosis. An 
apical systolic murmur, without other abnormal findings, 
is not evidence of disease of the heart. 

It is proverbially difficult to estimate slight degrees of 
diminished tolerance to exercise. As said in a previous 
chapter, it is not merely the production of symptoms on 
exertion, but of symptoms that are untoward for the par¬ 
ticular patient under examination. Experience is prob¬ 
ably the best guide in forming one’s judgment. The 
symptom of pain on exertion in this case became largely 
valueless as an indication of cardiac insufficiency, when on 


ILLUSTRATIVE CASE REPORTS 


337 


further investigation it was found to be a dragging sensa¬ 
tion in the abdominal wall. 

This patient’s physical development, or lack of it, offers 
a sufficient cause for her symptoms. The exaggerated 
curve of the spine and the pendulous abdominal wall are 
well-known physical handicaps. Her marital troubles 
would not conduce to the possession of good health. 

The above case also serves as an illustration of the pre¬ 
cept that the examiner must keep in mind the patient as a 
whole and not be too ready to blame the heart. Sir William 
Osier is often quoted as saying that he who thoroughly 
knows syphilis knows all medicine; with almost the same 
justification it may be stated that he who knows all cardi¬ 
ology must be familiar with all medicine. 


22 



CASE INDEX* 


Aneurism, 9 

Angina pectoris, 10, 12, 21 
simulation of, 22 
Aortic regurgitation, 4, 7, 8 
Argyria, 27 

Arteriosclerotic heart disease, 11, 12 
Asthma, 7 

Atrio-ventricular rhythm, 25 

Auricular fibrillation, 3, 5, 8, 14, 15, 16 

Autopsy, 6, 9, 17 

Blood culture positive, 6 

Capillary pulse, 4, 7 

Chest deformed, 14, 28 

Chill, 5, 6, 26 

Congenital heart disease, 17, 18 
coarctation of aorta, 17 
dextrocardia, 18 
patent ductus arteriosus, 17 
patent foramen ovale, 17 
patent interventricular septum, 17 
Corrigan pulse, 4, 7, 8, 9 
Cough, 3, 9, 15 

Cyanosis, 5, 7, 9, 14, 16, 23, 27 
Death, sudden, 14 
Diphtheria, 16 
Doubling of rate, 24 
Duroziez’s sign, 4 
Dysphagia, 9 

Dyspnoea (see shortness of breath) 
Edema, 5, 7, 9, 16 
slight, 4, 13, 15 
Effort syndrome, 19 
Electrocardiogram, auricular hyper¬ 
trophy, 3 
Emaciation, 5, 16 
Embolism, 6, 14 
Exercise tolerance, 29 
Extrasystoles, 3, 16, 26, 27 
" * The numbers refer to cases and 

not to pages. 


Family history, positive findings, 2 
Fever, 5, 6, 26 
Gallop rhythm, 16 
Gonorrheal arthritis, 7 
Heart-block, 9 

Heart failure, of definite degree, 2, 
3, 5, 7, 8, 9, 14, 15, 23 
Hemoptysis, 3 

Hypertensive heart disease, 13, 14, 21 
Hyperthyroidism, 15 
Impulse, diastolic, 2, 4 
diffuse 2, 4 

outside nipple line, 4, 5, 7, 8, 9, 13, 
14, 15, 19, 21 

systolic retraction of, 2, 4 
Irritable heart, 20, 25 
Liver, enlarged, 9, 23 
Mitral involvement, 1 
regurgitation, 1, 2, 3, 4 
stenosis, 2, 3, 4, 5 

Murmurs, absent, 6, 17, 18, 19, 21, 22, 
23, 24, 26, 27 
crescendo at apex, 5, 29 
diastolic at apex, 2, 3, 4, 5 
diastolic at base, 4, 7, 8, 9 
“ presystolic,” 5, 29 
pulmonic, 28 

systolic at apex, 1, 2, 3, 4, 7, 8, 9, 
11, 13, 14, 15, 16, 20, 25, 29 
systolic at base, 4, 7, 9, 10, 11, 12, 28 
“ Myocarditis,” 20 
Nephritis, 13 
Orthopnoea 2, 7, 14 
Pain, arm, 10, 12, 21 
jaw, 10 
neck, 10, 12 
precordia, 2, 10, 22 
shoulder, 2, 21 
side, 5, 6 

substernal, 10, 12, 21 


839 




340 


CASE INDEX 


Palpitation, 5, 11, 15, 19, 20, 22, 25 
Paroxysmal tachycardia, 23 
Pericardial adhesions, 4 
friction, 2 

Pericarditis, acute, 2, 6. 

Pistol-shot in artery, 4 
Premature beats, 3, 16, 26, 27 
Pulmonic murmur, 28 
second sound accentuated, 2, 5 
Pulsation, below left scapula, 2, 4 
suprasternal, 9, 12 
Pulse, capillary, 4, 7. 

Corrigan, 4, 7, 8, 9 
deficit, 3, 14 
pseudo-alternation, 26 
Rheumatic heart disease, 1, 2, 3, 4, 5 
Rhythm, atrio-ventricular, 25 
coupled, 26 
gallop, 16 


Rontgen findings, positive, 1, 8, 9, 10, 
12, 18, 21 

Septic heart disease, 5, 6 
Shortness of breath, 2, 3, 4, 7, 8, 9, 14, 
15, 23, 29 

Sino-auricular block, 24, 25 
Social history, 20 
Supracardiac dulness, 9, 10, 12 
Symptoms, absent, 1, 18, 24 
Syphilis, cardiovascular, 7, 8, 9, 10 
Thrill, at apex, 5, 11 
Traube’s double sound, 4 
Tricuspid lesion, 6 
Urine, red blood cells in, 6 
Visceroptosis, 1, 29 
Vomiting, 5, 16, 26 
Weakness, 5, 13. 


INDEX 


“A” wave, 51, 56, 57, 62, 211, 215 
Aberration of the ventricular waves, 
76, 77, 80 

Abortive beats (see pulse deficit) 
Abscissae, polygraph, 54 
electrocardiogram, 70 
A-C interval, 57, 62 
Aconitine, 197, 208, 213 
Activity of heart disease, 99, 102 
Adams-Stokes’ syndrome, 216, 256 
Adrenalin, 208, 213, 266 
test, 162 
Alcohol, 127, 267 

Allbutt, C. A., 126, 127, 142, 151, 186, 
187, 190 

Allen, F. M., 150, 153, 157 
Allen, H. B., 103 
Ammonia, 267 
Amyl nitrite, 41, 192, 267 
Anaphylaxis, 213 
Anemia, 123, 152 
Aneurism, 46, 123, 129, 241 
cardiac, 128, 244 
frequency, 137 
murmurs in, 133 
non-syphilitic, 130, 135 
ventricular, 128 

Angina pectoris, 45, 128, 137, 147, 152, 
155, 184 
diagnosis, 189 
etiology, 184 
mock, 190, 191 
predisposing causes, 193 
prognosis, 192 
symptoms, 187 
treatment, 192 
Anthrax, 135 
Aorta, 22 

calcification in, 129, 136 
coarctation, 174 
dilated, 35, 38, 47 


elongated, 35 
isthmus, 174 

Rontgen findings, 133, 134 
Aortic insufficiency, 32, 34, 39, 40, 111, 
113, 115, 128, 134, 136, 226, 237 
functional, 100, 229 
Aortic stenosis, 111, 113, 128, 174, 
230 

Aortic vestibule, 30 
Aortitis, 185, 186 
non-syphilitic, 135 
syphilitic (see cardiovascular syphi¬ 
lis) 

Apex, movement of, 24, 85 
impulse, 32, 33, 85, 152 
fixed, 112 

in mitral stenosis, 104 
retraction of, 104 
Aphasia, 122 
Aphonia, 110, 131, 173 
Apocynum, 265 
Arrhythmia, 92, 195 
absolute, 210 
combined, 83, 220 
effect of exercise on, 210 
respiratory (see sinus arrhythmia) 
Arsphenamine, 124, 138, 139, 141 
Arterial signs, 227, 228, 229 
Arteries, aorta (see) 
to bundle branches, 19 
carotid, visible pulsation, 32 
coronary, 19, 20, 82 
occlusion, 77 
sclerosis, 128, 185 
spasm, 185 
thrombosis, 190 

enlarged on back of abdominal 
cavity, 174 

internal mammary, 21, 239 
“pipe-stem,” 145 
pulmonary, 21 


341 


34* 


INDEX 


Arteriosclerosis 135, 1S5, 20S 
Arteriosclerotic heart disease, 142 
blood pressure in, 145 
diagnosis 146 
etiology, 142 
pathology, 143 
prognosis, 147 
symptoms and signs, 144 
treatment, 147 
Aschoff bodies 98 
Asphyxia, 213 
Atropine, 196, 216, 21S 
Auricle, left, 16 

enlargement of, 3S 
right, 15, 37 

enlargement of, 32 
Auricular appendix left, 16 
right, 16 

Auricular fibrillation (see fibrillation) 
Auricular flutter (see flutter) 
Auricular systole, 23 
Auriculo-ventricular bundle, 18 
branches 19 
rhythm, 57, 75 
Auscultation, 39, 40 
direct, 40 

“B" wave, 56, 215 
Bainbridge, F. A., 28 
Bamberger's sign. 238 
Barium chloride, 197, 208, 267 
Baths, 1-58, 252 
Bayliss and Starling, 66 
Benda. 126 
Bennert. R., 135 
Benzyl benzoate, 159 
Billings, 124 

Bleeding (see venesection) 

Block, arborization, S3 

auriculo-ventricular (see heart- 
block) 

intraventricular, S2, S3 
sino-auricular, 58. 75, 196 
Blood, chemistry, 153 


cultures, 123, 124 
flow, velocity of, 230 
white count, 123 
Blood pressure, 90, 219 
in aortic insufficiency, 42 
in cardiovascular syphilis, 133 
determination, 42, 43 
effect of digitalis, 257 
elevated, 152 
fall, 190 

femoral, 43, 90, 228 
hydremia, 254 
instruments, 42 
pulse pressure, 90 
Books, 158 
Bowels. 157, 252 
Bowie, 39 

Broadbent's sign, 112 
Broken compensation (see heart 
failure) 

Bromides, 200, 204 
Brooks, H.. 128 
Brugsch and Schittenhelm, 38 
Bundle of His (see auriculo-ventric¬ 
ular bundle) 

Burton-Opitz, R., 107 

“C” wave, 54 
Cacodylate of soda, 124 
Cactin, 267 
Caffein, 266 

Caffein sodiobenzoate, 268 
Calcification of aorta, 136 
Camphor, 267 
Capillary electrometer, 66 
Carcinoma of heart, 238 
“Cardiac neurosis'’ (see effort 
syndrome) 

Cardio-thoracic ratio, 46, 90 
Cat unit (see digitalis) 

Cautley, E. 172 
Cerebral hemorrhage, 151 
Chill, 120, 121 

Chloroform, 164, 197, 208, 266 


INDEX 


343 


Chordae tendineae, 17, 98 
Chorea, 31, 97, 119 
Christian, H. A., 259 
Circus movement, 201, 205, 209, 2G8 
Classification of heart disease, 91 
New York, 93 
Claudication, 186 
Climate, 253 
Clothing, 253 
Coffee, 198 

Congenital heart disease, 170 
symptoms, 170 
treatment, 174 
Constipation, 157 
Contour of heart, 36, 47 
Contraction, amplitude of, 28 
law of, 26 
wave, 25, 72 

Conus arteriosus, 16, 21, 38, 235 
Convallaria, 265 
Convulsions, 122, 170 
Cor bovinum, 227 
Coronary artery (see arteries) 
sinus, 18, 20 
valve, 20 

Corpus Aurantii, 17 
Cotton, T. F., 73, 236 
Cough, 31 
brassy, 131 

Councilman, Mallory, and Pearce, 165 
Coupled rhythm (see pulse, bigemi¬ 
nal) 

Crampton, C. W., 44 
Curran, 19 

Cushney, Marris, and Silberberg, 257 
Cyanosis, 32, 170 

“ D. A. H.” (see effort syndrome) 
Da Costa, J. M., 175 
Danzer, C. S., 46 

Death, sense of impending, 187, 189 
sudden, 155, 168, 187, 188 
Dextrocardia, 170 
Diabetes, 149, 153, 156 


Diastasis, 24 
Diastole, 24 
Dicrotic notch, 55, 56 
Diet, 252 

during administration of mer¬ 
cury, 139, 140 
in arteriosclerosis, 148 
in hypertension, 156 
Digitalis, 117, 148, 169, 197, 204, 207, 
208, 212, 257, 270 
administration, 260 
cat unit, 260 

effect on electrocardiogram, 72, 258 
Eggleston method, 260 
intramuscularly, 265 
preparation, 258, 264 
standardization, 259 
T wave in, 72, 258 

Dilatation of heart, 28, 236, 239, 254 
Diphtheria, 135, 213 
Diphtheria, the heart in, 165 
diagnosis, 168 
etiology, 165 
pathology, 165 
prognosis, 168 
symptoms, 166 
treatment, 169 
Diuretics, 155, 157, 268 
Diuretin, 155, 268 
Dizziness, 145, 179 
Dominant rhythm, 53, 59, 62 
Double shock, 35 
Dress, 253 

Dropped heat (see heart-block) 
Drury and Uiescu, 272 
Ductus arteriosus (Botalli), 29 
patent, 171, 173 
Dulness, apex left lung, 106 
cardiac, 37, 38, 85 
deep, 38, 86 

left border, 37, 38, 86, 105 
right border, 37, 86, 105 
superficial, 38, 86 
below scapula, 238 


344 


INDEX 


supracardiac, 38, 87, 132, 145, 173 
beside thoracic spine, 132 
Duroziez’s sign, 229 
Dyspnoea, 32 
treatment, 254 

Ectopia cordis, 171 
Edelmann, 66 

Edema, 33, 152, 155, 184, 252, 255 
Edwards, A. R., 98 
Effort syndrome: irritable heart, 175 
diagnosis, 177 
etiology, 175 
prognosis, 177 
symptoms and signs, 176 
treatment, 178 
Eggleston, C., 260 
Einthoven, W., 66, 67, 68 
triangle, 69 

Electrocardiogram, 154 
in dextrocardia, 171 
in mitral stenosis, 110 
normal, 69 
standardization, 68 
Electrocardiography, 64 
history, 65 
the instrument, 67 
value of, 64 
Electrodes, 67 
Embolism, 110, 122, 167, 271 
“crossed or paradoxical,” 173 
septic, 120 
Embryology, 29 
Emphysema, 86 
Empyema, 119 
Endocarditis 
acute, 225 

bacterial (see septic heart disease) 
infectious (see septic heart disease) 
malignant (see septic heart disease) 
statistics, 98, 111 

ulcerative (see septic heart disease) 
Enlargement of heart, 112, 152, 227, 
236 


of left ventricle, 32, 38 
of right heart, 32, 184 
of right ventricle, 25, 34, 38, 104 
Epigastric pulsation, 32, 104, 237 
Epinephrin (see adrenalin) 
Epistaxis, 152, 170 
Erysipelas, 135 
Erythrol tetranitrate, 194 
Eustachian valve, 29 
Ewart’s sign, 238 
Ewing, E. M., 54 
Examination, methods of, 31 
Exercise, 41, 178, 188, 249 
effect on arrhythmias, 199, 200 
physiology of, 27, 218 
tolerance, 31, 43, 45, 93, 177, 183 
Extrasystole, 52, 53, 58, 146, 197 
auricular, 58, 59, 76 
differential diagnosis, 199 
etiology, 197 
interpolated, 58, 219 
nodal, 59, 76 
pause after, 59 
prognosis, 200 
symptoms and signs, 198 
treatment, 200 
ventricular, 58, 59, 77, 221 
Eye, fundus of, 153 

Facies, 104 
Fatigue, 31, 183 
Fever, irregular, 122, 130 
“FF” waves, 61 

Fibrillation, auricular, 54, 57, 61, 78, 
146, 167, 208, 268 
diagnosis, 211 
etiology, 208 

flutter-fibrillation type, 79 
pathology, 210 
prognosis, 212 
symptoms and signs, 210 
treatment, 212 

Fibrillation, ventricular, 80, 187, 258, 
266 


INDEX 


345 


Fingers, clubbing of, 104, 170 
painful areas in, 122 
Fleming and Kennedy, 166 
Flint, Austin, 39, 109 
Fluid intake, 157, 252, 255 
Flutter, auricular, 61, 62, 78, 202, 205, 
268 

diagnosis, 206 
etiology, 205 
impure, 79 
prognosis, 207 
symptoms and signs, 206 
treatment, 207 

Focus of infection, 97, 114, 116, 175, 
178, 247 

Foramen ovale, 29 
closure of, 173 
patent, 172 
Frey, W., 271 
Friction at base, 132 
pericardial, 35, 238 
pleuro-pericardial, 239 
Friedreich, 112 
Functional conditions, 183 
Fundus of eye, 153 

Gallop rhythm, 35, 167, 215 
Gangrene, 122 
Gannet, 40 
Gaskell, 27 

Gastric symptoms, 151, 255 
treatment, 193 
Gonorrhea, 119, 135 
Goodpasture, E. W., 160, 161, 164 
Graham Steell murmur, 109 
Graphic methods, 49 
Gross, L., 82 
Gummata, 128 

“H” wave, 56, 215 
Hands, cyanosis of, 176 
pain in, 122, 188 
Harding, M. E., 167 
Hart, T. S., 266 


Hatcher and Brody, 260 
Hay, J., 51 

Headache, from cerebral congestion, 
144, 147 

Heart, anatomy, 15 
low-lying, 32, 47 
normal, 84 
normal position, 15 
Heart-beat, cessation of, 214, 215 
mechanism, 25 

Heart-block, 61, 75, 78, 80, 133, 134, 
147, 166, 168, 199, 206, 213 
complete, 62, 80 
diagnosis, 216 
etiology, 213 
partial, 61, 80 
pathology, 214 
prognosis, 217 
symptoms and signs, 214 
treatment, 217 

Heart disease, active or inactive, 99, 
102 

in anemia, 92 
beer heart, 92 
classification, 91 
in obesity, 92 
potential, 113, 134 
reliable signs of, 48 
tumors, 92 

types of (etiological), 91 
Heart failure, 31, 45, 92, 183, 192, 234 
relation to infection, 100, 183 
Heat, 192 
Hellebore, 265 
Hemiplegia, 122, 271 
Hemopericardium, 240 
Hemoptysis, 106, 110 
Henderson, Y., 107 
Henderson and Barringer, 28 
Henderson and Johnson, 23 
History, 31, 84, 97, 136, 203 
etiological diseases, 31 
Hoarseness, 110, 131 
Hoffman’s anodyne, 193 


346 


INDEX 


Hoover, C. F., 38 
Hopkins, A. H., 150 
Huchard’s table, 190, 191 
Hydremia of blood, 254 
Hyperesthesia, 176, 177 
Hyperpiesis (see hypertensive heart 
disease) 

Hypertension, effects of digitalis on, 
258 

Hypertensive heart disease, 136, 149, 
219 

diagnosis, 154 
etiology, 149 
pathology, 150 
physical signs, 152 
prognosis, 155 
symptoms, 151 
treatment, 156 
Hyperthyroidism, 149, 161 
Hyperthyroidism, the heart in, 160, 
177, 208 
diagnosis, 163 
etiology, 160 
pathology, 160 
prognosis, 164 

symptoms and physical signs, 161 
treatment, 164 
Hypertrophy, 236 
ventricular, 73 
Hypothyroidism, 72 

Idio-ventricular rhythm, 81 
Impulse, aortic, 35 
cardiac (see apex) 
absent, 239 
character, 34 
diastolic, 34 
downward, 237 
maximum, 33, 85 
movement of, 33 
out and downward, 34, 227, 237 
position, 33, 34 
retraction of, 34 


Indigestion, 31 
“acute,” 188 
Infarcts, 122 
of myocardium, 77 
Infection (see focus of) 

Influenza, 121, 135, 185 
Infundibulum (see conus arteriosus) 
Inman, T. G., 145, 148 
Insomnia, 255 
Inspection, 32 

Interventricular septum, 30 
patent, 30, 171, 173 
Iodide of potassium, 135, 140 
Irregularity (see arrhythmias) 
Ischemia (see myocardium) 

Isometric period, 25 

Jaundice, 104 

Kidney, function of, 153, 154 
Kolliker and MUller, 65 
Krumbhaar, E. B., 162 

Lancisi, 126 

Lead, 142 

Leads, 68 

“Leaky valves,” 251 

Lesions, structural, 93 

Levison, L. A., 125 

Levy, A. G., 266 

Lewis, T., 24, 45, 48, 50, 53, 56, 61, 
64, 67, 68, 72, 81, 176, 178, 197, 
200, 202, 205, 206, 207, 208, 209, 
213, 214, 217, 236 
Lewis, Drury, and Uiescu, 272 
Lewis, Meakins, and White, 81 
Lewis, Feil, and Stroud, 205, 207, 209 
Ligamentum arteriosum, 21 
Litten’s sign, 112 
Liver, pulsation, 234 
swelling of, 184, 202, 234 
Ludwig, angle of, 33 

MacCallum, W. G., 17, 143 


INDEX 


Mackenzie, J., 49, 97, 112, 187, 225, 
234, 235 

Magnus-Alsleben, 166 
Malaria, 135 
Massage, 250 
of heart, 256 
McCrae, 98 
Meakins, J. C., 81 
Meakins and Gunson, 178 
Means, J. H., 162 
Measles, 97, 135 
Mediastinal tumors, 137 
Meningitis, purulent, 121 
Mercury, 135, 139, 141 
Metabolism, basal, 154, 162 
Mines, G. A., 206 
Mitral insufficiency, 102, 115, 231 
relative, 132, 231, 232 
Mitral stenosis, 34, 38, 39, 88, 99, 
103, 115, 136, 208 
facies, 104 
murmurs, 107 
Monckeberg’s sclerosis, 143 
Morphine, 193, 213 
Moschcowitz, E., 151 
Muller, F., 142, 163 
Murmurs, 40, 41, 121, 225 
apical, 41, 89 
Austin Flint, 132 
basal, 41, 89 
crescendo, 88, 108 
diastolic, 39 

at base, 100, 226 
double, 172 

experimentally produced, 172 
Graham Steell, 109 
mid-diastolic, 233 
in mitral stenosis, 107 
pitch, 39, 40 
presystolic, 107, 108 
production of, 106 
systolic, at apex, 103, 132, 146, 153, 
176 

at aortic area, 132 


347 

at pulmonary area, 89, 172, 234 
timing of, 34 
tricuspid, 233 
Muscarine, 197, 213 
Musser, J. H., Sr., 192 
Myocarditis, 235 
toxic, 160, 165 

Myocardium, 97, 98, 115, 127, 212, 235 
anatomy, 17 

compensatory circulation, 185 
degenerative changes, 144 
in hypertension, 151 
in hyperthyroidism, 160 
ischemia, 185, 186, 191 
in mitral stenosis, 103 
Myogenic theory, 26 

Nephritis, 122, 150, 153, 156, 238 
Nerves, 20, 26 
phrenic, 21 

recurrent laryngeal, 22, 110, 131, 173 
sympathetic, 21, 26, 243 
vagus, 21, 26, 29, 195, 196, 203, 213, 
216, 217, 257, 267, 269 
“Nervous heart” (see effort syn¬ 
drome) 

Nervousness, 204 

Neuro-circulatory asthenia (see 
effort syndrome) 

Nicotine, 197, 208, 213 
Nitrites, 267 

Nitroglycerine, 159, 192, 194, 267 
Nodding of head, 228 
Node, auriculo-ventricular, 18 
sino-auricular, 17, 25 
Tawara, 18 

Nodules, subcutaneous, 101 
Obesity, 151, 155 

Ophthalmoscopic examination, 153 

Ordinates, 70 

Orr and Innes, 157 

Osier, W., 190 

Ouahain, 266 


348 


INDEX 


Output of heart, 27 
Overeating, 155 

“P” wave, 71, 76, 77, 78, 80 
absent, 75, 76, 79 
diphasic, 71 
inverted, 71, 75, 77 
in mitral stenosis, 110 
normal, 71 
notched, 71 

time before contraction, 72 
Pain, 31, 183 

in angina pectoris, 187, 188 
in cardiovascular syphilis, 130 
diiferential diagnosis, 187 
in hand, 188 
in left arm, 176 
in leg, 145 
precordial, 101, 176 
treatment, 253 
Pallor around mouth, 167 
Palpation, 33 
Palpitation, 31, 179, 202 
Panophthalmia, 121 
Papillary muscles, 17, 19 
Pardee, H. E. B., 89, 191, 260 
Parkinson, J., 168 

Paroxysmal tachycardia, 60, 76, 163, 
177, 183, 201, 206 
diagnosis, 202 
etiology, 201 
pathology, 201 
prognosis, 203 
symptoms and signs, 201 
treatment, 203 
ventricular type, 77 
Passive motions, 250 
Pause, post-systolic, 199, 210 
compensatory, 199 
Peabody, F. W., 48 
Peabody, Sturgis, Thompkins, and 
Wearn, 162 
Percussion, 35, 38, 87 
limitations, 35, 87 


Pericarditis, 115 
acute, 237 

adhesive, 34, 112, 240 
with effusion, 38, 101, 115 
rub, 101 

Pericardium, 21 
paracentesis, 239 
surgical drainage, 240 
Peripheral vessels, in exercise, 27 
Petechiae, 123 
Phonocardiography, 88 
Physiology, 22 

cardiac cycle, 22, 23 
functions of heart muscle, 27 
Physostigmine, 197, 213 
Pistol-shot sound (see sounds) 
Pituitary extract, 267 
Place, E. H., 168 
Plesch, 38 

Pneumonia, 31, 119, 121, 135, 142, 154 
Pneumopericardium, 240 
Polycythemia, 170, 233 
Polygram (see individual waves) 
analysis, 54, 56 

arteriogram, respiratory variation 
of, 52 

artifact in, 56 
exaggerated waves, 56, 62 
phlebogram, 54 
Polygraphs, types, 49 
vibration frequency, 50 
Polygraphy, 49, 64 
Porter, W. T., 107 
Position of patient (see posture) 
Posture of patient, 38, 41, 211, 218, 
238 

effect of change of, 112 
effect on rate, 202 
of baby, 173 

Potassium iodide, 140, 243 
salts, 197, 208, 213 
Potential heart disease, 113, 134 
P-R interval, 57, 71, 80 
Pratt, F. H., 186 


INDEX 


349 


Precordia, bulging of, 32, 170 
Premature beat (see extrasystole) 
Preponderance, ventricular, 73, 83, 
110, 154, 237 
index, 73 

Pressure curves, 24 
intra-auricular, 107 
intraventricular, 107 
Price and Mackenzie, 166 
Protodiastolic sound, 109 
Psychic aspects, 250 
Ptosis of heart, 47 
Puerperal sepsis, 31, 97, 119 
Pulmonary insufficiency, 172, 234 
stenosis, 171, 234 
veins, 16 

Pulmonic valve, palpable closure of, 
35 

Pulsation, carotid, 32 
epigastric, 32, 104, 237 
expansile, 132, 242 
second and third interspaces, 131 
suprasternal, 131 

Pulse, alternation (see pulsus alter- 
nans) 

anacrotic, 60, 231 
bigeminal, 52, 219, 220, 258 
bisferiens, 231 
capillary, 228 

Corrigan, 105, 136, 173, 227, 229 
deficit, 209, 210, 212 
paradoxical, 53, 112 
plateau, 231 

pseudo-alternation, 52, 219 
respiratory variation in, 52 
tracings (see polygram) 
venous, 234 

auricular form, 57 
inspection of, 211, 215 
ventricular form, 57, 61, 210 
wave, velocity of, 230 
Pulsus alternans, 52, 219 
Pulsus paradoxus (Kussmaul’s pulse), 
53, 112 


Pupils, unequal, 131 
Purkinje fibres, 19 
Pustules, 120 

“Q” Wave, 71 

QRS complex, 69, 71, 82 

Quinidine, 207, 213, 268 

“R” wave, 71, 73, 74 
notched, 72 
prolonged, 72, 82 
thickened, 72 

time before contraction, 72 
Rash on skin, 120, 122 
Rate, 28, 62, 78, 81, 202, 210, 215, 270 
acceleration, 198, 200 
relation to arrhythmias, 199 
doubling of, 196 
halving of, 196 
rule of, 211 
Ray fish, 205 

Reid, W. D., 25, 89, 108, 111, 126, 127, 
135, 138 

Renal function, 152, 154 
Respiration, paralysis, 271 
whistling, 131 
Rest, 193 

in bed, 115, 140, 148, 169, 248 
Restlessness, 253 
Resuscitation of heart, 256 
Retraction, of cardiac impulse, 32, 
104 

of chest wall. 111 
Reuta, 126 

Rheumatic fever, 19, 97, 119, 135, 185 
Rheumatic heart disease, 97, 136 
Aschoff bodies, 98 
diagnosis, 113 
etiology, 97 
pathology, 98 
prognosis, 114 
symptoms, 99 
treatment, 115 


350 


INDEX 


Rhythm, coupled, 258 
dominant, 53, 59, 62 
gallop, 35, 167, 215 
idio-ventricular, 81 
two to one, etc., 206 
Robinson and Hermann, 77 
Robinson and Wilson, 258 
Roll in mitral stenosis, 108 
Rontgen findings, 38, 46, 90, 110, 133, 
145, 231, 239 

comparison with percussion, 37 
Rotch’s sign, 238 
Rumble in mitral stenosis, 108 
Rupture of heart, 240 

“S” wave, 71 

Sallowness of complexion, 123 
Salt, 150, 156, 255 
Scarlet fever, 31, 97, 135, 160 
Schmorl, 126 
Schneider, E. C., 253 
Sears’ point, 240 
Sedatives, 158, 200, 204 
Septic heart disease, 119, 135 
acute type, 120 
chronic type, 121 
diagnosis, 123 
etiology, 119 
pathology, 119, 125 
prognosis, 124 
symptoms, 120 
treatment, 124 
Septicemia, 124 

Septum, patent interventricular, 171, 
173 

Serum therapy, 125 
Shattuck, G. C., 35 
Shortness of breath, 31, 183 
Sign, Bamberger’s 238 
Broadbent’s, 112 
Duroziez’s, 229 
Ewart’s, 238 
Litten’s, 112 
Rotch’s, 238 


Sino-auricular block, 58, 75, 196 
Sinus arrhythmia, 53, 57, 74, 195 
phasic type, 58, 74 
Sinus of Valsalva, 17, 20 
Sinus venosus, 15 

Size of heart, 36, 46, 86, 93, 202, 236 
cardio-thoracic ratio, 46, 90 
Skin, petechise, 123 
pustules, 120 
rashes, 120, 122 
syphilitic lesions, 134 
Small-pox, 135 
Smith, S. C., 167 
Sodium nitrite, 194 
“Soldier’s heart” (see effort syn¬ 
drome) 

Sounds, 25, 41, 88 
aortic, 88 

auricular, 199, 206, 207, 215 
first, 25, 72, 88, 108 
first, split, 88, 176 
pistol-shot, 228 
protodiastolic, 109 
pulmonic, 88 
second, 25, 72, 88, 108 
accentuated, 88 
aortic, 132, 146, 231 
reduplicated, 89, 109 
split, 88, 176 
third, 57, 89, 109 
timing of, 34 
Traube’s, 229 
Southey’s tubes, 255 
Space, deep cardiac, 86 
superficial cardiac, 86 
Spartein, 267 
Spas, 252 

Spleen, enlarged, 120 
infarct, 122 
Squill, 265 

Standstill, cardiac, 256 
ventricular, 214 

Starling, E. H., 24, 43, 66, 107, 228 
Steell, Graham, 109, 111 


INDEX 


351 


Stethoscope, 39, 227, 

Stewart, H. A., 229 

Strophanthin, 197, 208, 213, 265, 266 

Stroplianthus, 265 

Structural lesions, 225 

Strychnine, 267 

Sweats, 122 

Symptoms, 31 

Syphilis, 185 

Syphilis, cardiovascular, 126, 208, 218, 
242 

blood pressure in, 133 
congenital, 127 
diagnosis, 134 
etiology, 126 
frequency of, 126 
mitral stenosis, 103 
pathology, 127 
physical signs, 131 
prognosis, 137 
symptoms, 130 
therapeutic test, 135 
treatment, 138 

“T” wave, 72, 162, 258 
flattened, 72 
inverted, 72 
normal, 72 
Tabes dorsalis, 137 
Tachycardia, differential diagnosis, 
177 

effort syndrome, 163, 177 
hyperthyroidism, 161 
(see paroxysmal tachycardia) 
regular, 202 
Tea, 198 

Teeth, 97, 117, 188 
Thayer, W. S., 89 
Thayer and MacCallum, 172, 229 
Thebesius, veins of, 20, 186 
Theobromin sodium salicylate, 155, 
268 

Theocin, 155, 266, 268 
Theophyllin, 197 


Theophyllin sodioacetate, 155, 268 
Therapeutic test, 135 
Thrill, 34, 85, 231 
at apex, 105 

at base, 132, 172, 173, 174 
Thrombosis, 110, 166 
Thyroid heart (see hyperthyroidism) 
Time marker, 55, 70 
Tobacco, 190 (see nicotine) 
Tonsillectomy, 117, 248 
Tonsillitis, 31, 97, 119 
Tracheal tug, 242 
Transfusion of blood, 125 
Traube’s sounds, 229 
Treatment, drug, 257 
etiological, 247 
exercise, 118 
general, 248 
regulation of life, 118 
symptomatic, 118, 253 
Tricuspid insufficiency, 233, 234 
relative, 234 
Tricuspid stenosis, 233 
Tuberculosis, 135 
of heart, 114, 238 
miliary, 123 
pulmonary, 137, 170 
Typhoid fever, 123, 135, 142 

“U” wave, 72 

“V” wave, 55 
Valves, 16 

Vaquez and Bordet, 202 
Veins, anterior cardiac, 20 
cervical, 32 

diastolic collapse, 112 
engorgement, 131, 184 
inspection of, 211, 215 
pulmonary, 16 
of Thebesius, 20, 186 
Venesection, 158, 254 
“bloodless,” 255 


INDEX 


352 

Ventricle, left, 16 
right, 16 

Ventricular escape, 75, 80, 258 
filling, 107 
output, 27 
systole, 23, 25 
Veronal, 200, 204 
Vital capacity, 47 
Vomiting, 169, 203, 204 

Walker, R. W. S., 173, 227 
Waller, A. D., 66 
Walton, G. L. W., 158 
Warthin, A. S., 126, 127, 129 
Wassermann reaction, 133 


Water (see fluid intake) 
amount of, 157 
Weiss and Hatcher, 265 
Wenkebach, 49 
White, B., 125 
White, P. D., 219, 265 
White and Aub, 162 
White and Bock, 73 
Wiggers, C. J., 25, 50, 229 
Williams, 67 
Williamson, C. S., 238 
Wilson and Hermann, 72, 73, 83, 237 
Worry, 151, 158 

Zollinger, F., 229 

























